Endovascular treatment of traumatic oronasal hemorrhage complicated with progressive acute epidural hemorrhage: A case report.

RATIONALE: Massive oronasal hemorrhage can induce shock and is life-threatening, and early endovascular treatment is the standard of care. Few studies have reported the use of endovascular treatment for acute epidural hemorrhage (AEDH). However, endovascular treatment of oronasal hemorrhage complicated by AEDH has not yet been demonstrated. Many patients with a low to moderate volume of oronasal hemorrhage complicated by AEDH choose conservative treatment but eventually undergo craniotomy due to increased intracranial hemorrhage. PATIENT CONCERNS: A 32-year-old man presented to our hospital with traumatic oronasal hemorrhage complicated by AEDH after being hit by a blunt object. DIAGNOSIS: Computerized tomography suggested progressive AEDH and multiple basilar skull fractures. Emergency cerebral angiography showed rupture of the right middle meningeal artery and a branch of the left maxillary artery causing AEDH and oronasal hemorrhage. INTERVENTIONS: The patient underwent interventional embolization to treat the ruptured intracranial vessels. OUTCOMES: After 23 days, cranial computerized tomography showed remarkable absorption of the right frontal epidural hematoma, with the patient having a Glasgow Coma Scale score of 15. LESSONS: This case provides a valuable treatment for patients with AEDH complicated with oronasal hemorrhage, early interventional embolization may be an effective treatment strategy to prevent further complications and ensure a good patient outcome.

The Neuroprotective Effects of Necrostatin-1 on Subarachnoid Hemorrhage in Rats Are Possibly Mediated by Preventing Blood-Brain Barrier Disruption and RIP3-Mediated Necroptosis.

Despite the substantial efforts to elucidate the role of early brain injury in subarachnoid hemorrhage (SAH), an effective pharmaceutical therapy for patients with SAH continues to be unavailable. This study aims to reveal the role of necroptosis after SAH, and explore whether the disruption of the blood-brain barrier (BBB) and RIP3-mediated necroptosis following SAH in a rat SAH model are altered by necrostatin-1 via its selective inhibition of receptor-interacting protein kinase 1 (RIP1). Sixty-five rats were used in the experiments. The SAH model was established using endovascular perforation. Necrostatin-1 was intracerebroventricularly injected 1 h before SAH induction. The neuroprotective effects of necrostatin-1 were evaluated with multiple methods such as magnetic resonance imaging (MRI) scanning, immunohistochemistry, propidium iodide (PI) labeling, and western blotting. Pretreatment with necrostatin-1 attenuated brain swelling and reduced the lesion volume on T2 sequence and ventricular volume on MRI 72 h after SAH induction. Albumin leakage and the degradation of tight junction proteins were also ameliorated by necrostatin-1 administration. In addition, necrostatin-1 decreased the number of PI-positive cells in the basal cortex, reduced the levels of the RIP3 and MLKL proteins, and inhibited the production of the pro-inflammatory cytokines IL-1ß, IL-6, and TNF-α. Based on the findings from the present study, the selective RIP1 inhibitor necrostatin-1 functioned as a neuroprotective agent after SAH by attenuating brain swelling and BBB disruption. Moreover, the necrostatin-1 pretreatment prevented SAH-induced necroptosis by suppressing the activity of the RIP3/MLKL signaling pathway. These results will provide insights into new drugs and pharmacological targets to manage SAH, which are worth further study.

Inhibiting of RIPK3 attenuates early brain injury following subarachnoid hemorrhage: Possibly through alleviating necroptosis.

Necroptosis is an inflammatory form of cell death that depends on receptor-interacting serine-threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) and displays the morphological characteristics of necrosis. To date, it is unclear to what extent necroptosis contributes to subarachnoid hemorrhage (SAH) induced brain injury. The present study aimed to investigate the RIPK3-mediated necroptosis and the effects of the RIPK3 selective inhibitor GSK'872 in early brain injury following SAH. After SAH, RIPK3 expression increased as early as 6 h and peaked at 72 h. Double immunofluorescence staining revealed that RIPK3 was mainly located in neurons. Most necrotic cells were neurons, which were further confirmed by TEM. Intracerebroventricular injection of GSK'872 (25 mM) could attenuate brain edema and improve neurological function following SAH and reduce the number of necrotic cells. In addition, GSK'872 could also decrease the protein levels of RIPK3 and MLKL, and cytoplasmic translocation and expression of HMGB1, an important pro-inflammatory protein. Taken together, the current study provides the new evidence that RIPK3-mediated necroptosis is involved in early brain injury and GSK'872 decreases the RIPK3-mediated necroptosis and subsequent cytoplasmic translocation and expression of HMGB1, as well as ameliorates brain edema and neurological deficits.

The 90-day prognostic value of serum cyclophilin A in traumatic brain injury.

BACKGROUND: Cyclophilin A is involved in many inflammatory diseases and its expression is up-regulated after brain injury. We determined if serum cyclophilin A could be used as a marker for severity and 90-day outcome in patients with traumatic brain injury (TBI). METHODS: Serum cyclophilin A concentrations were quantified in 105 severe TBI patients and 105 healthy individuals. Its association with Glasgow Coma Scale (GCS) score, 90-day mortality and 90-day poor outcome (Glasgow Outcome Scale score of 1-3) were investigated. RESULTS: Serum cyclophilin A concentrations were significantly higher in TBI patients than in healthy individuals. Cyclophilin A concentrations had a close relation to GCS scores and showed a high discriminatory ability for 90-day mortality and poor outcome according to area under receiver operating characteristic curve (AUC). Its AUC was in the range of GCS scores. Moreover, its combination with GCS scores significantly improved the predictive performance of GCS scores alone. In addition, serum cyclophilin A emerged as an independent predictor for 90-day mortality, overall survival and poor outcome. CONCLUSIONS: Increased serum cyclophilin A concentrations could reflect trauma severity and unfavorable outcome after head trauma, substantializing cyclophilin A as a potential biomarker for prognostic prediction of TBI.

[The expression and significance of apoptosis related gene BAG-1 in meningioma].

OBJECTIVE: To analyze the expressions of BAG-1 in meningioma for further understanding of biological behaviors of meningiomas. METHODS: The specimens included in this study were collected from 158 meningioma cases. Streptavidin-peroxidase were used in immunohistochemical staining. The results of immunohistochemical score were depending on the positive ratio and intensity of the immunoreactivity. The expressions of BAG-1 in meningioma were analyzed in relationship with histopathologic grading, postoperative recurrence. RESULTS: The difference in the expression degree of BAG-1 between each subtype in the same histopathologic grade and various subtypes between the grade of II to III were not statically significant (P > 0.05). The expression degree of BAG-1 between each subtype in the pathological grade I to the each subtype pathological grade I or III was different, the difference had statistical significance (P < 0.05 or P < 0.01). The immunohistochemical score of the expression of BAG-1 was decreased gradually with the pathologic grading of WHO increased, and the result was statistically significant (chi2 = 141.49, P < 0.01). As the immunohistochemical score of the expression of BAG-1 decreased the postoperative meningioma was easy to recur, the result was statistically significant (x2 = 55.13, P < 0.01). CONCLUSION: The expression degree of BAG-1 is in close correlations with the WHO pathologic grading of meningioma. The lower the expressions of BAG-1, the more recurrent with postoperation of meningiomas will be.

Expression and significance of E-cadherin and ß-catenins in pituitary adenoma.

This study used immunohistochemical methods for detecting the expression of E-cadherin and ß-catenin in pituitary adenoma. Specimens were collected from 91 cases. EnVision was used for immunohistochemical staining. The results were graded depending on the staining intensity and range. Associations between E-cadherin and ß-catenin expression and tumor subtype, invasiveness, and postoperative recurrence were investigated. There was a significant downregulation of E-cadherin and ß-catenin in growth hormone (GH)-type tumors when compared with prolactin-type tumors (u(c) = 2.693 and 2.109, respectively; P < .05). E-cadherin and ß-catenin were downregulated in invasive pituitary adenomas (u(c) = 3.563 and 4.166, respectively; P < .05) and in clinically recurring pituitary adenomas (u(c) = 2.871 and 3.866, respectively; P < .05). There was no difference in the percentage of invasive prolactin and GH secreting tumors (28.57% and 22.86%, respectively; P > .05). The expression of E-cadherin and ß-catenin in pituitary adenoma was significantly downregulated and related to subtype, invasiveness, and postoperative recurrence.

BAG-1 expression in human meningioma and correlation with clinical characteristics.

The aim of this study is to investigate BAG-1 expression in human meningiomas and to assess its association with pathological and clinical characteristics. BAG-1 expression was analyzed in 158 specimens of meningiomas using immunohistochemical staining, and the results were graded according to the positivity ratio and the staining intensity. We examined the correlations between BAG-1 expression and the 2007 WHO pathological classification, peritumoral edema and postoperative recurrence. There were no significant differences in BAG-1 expression among meningioma subtypes within the same histopathologic grade, as well as between grades II and III. BAG-1 expression in grade I was much higher than in grade II (P < 0.05) or III (P < 0.01). BAG-1 expression was gradually decreased with increasing WHO pathologic classification (χ (2) = 141.49, P < 0.01), as well as with the increase in peritumoral edema (χ (2) = 43.93, P < 0.01) and postoperative recurrence (χ (2) = 55.13, P < 0.01). BAG-1 expression in meningioma depends upon WHO pathologic classification and is decreased in higher tumor classification. It is associated with heavier peritumoral edema and more postoperative recurrences.

[MALDI-TOF-MS combined with WCX technique in diagnosing pituitary adenoma].

OBJECTIVE: Application of matrix assisted laser desorption ionization time of flight mass spectrometry enhancement (MALDI-TOF-MS) combined with WCX nanometer magnetic bead technique, screening of the serum biomarkers in pituitary adenoma, to establish a serum protein fingerprint classification decision tree. METHODS: Analyse the serum samples of 40 cases of pituitary adenoma and 60 cases of healthy adult and find the different protein peaks, then to establish the diagnosis model and the classification decision tree of pituitary adenomas. RESULTS: A total of 42 differences in protein peaks were identified in the experimental and control group (P < 0.01). The diagnosis model of pituitary adenomas was established by three protein peaks (3382.0, 4601.9, 9191.2). The model could screen the pituitary adenoma out of the normal population. The sensitivity was 90.00% and the specificity was 88.30%. By the double blind experimental validation, the model could diagnose the pituitary adenoma and the sensitivity was 88%, the specificity was 83.30%. CONCLUSION: Significantly different protein peaks can be screened out between pituitary adenoma cases and healthy controls using MALDI-TOF-MS combined with WCX technique, and these protein peaks may be used as a pituitary adenoma detection, follow-up indicator.

Pituitary adenoma biomarkers identified using proteomic fingerprint technology.

OBJECTIVE: To determine whether pituitary adenomas can be diagnosed by identifying protein biomarkers in the serum. METHODS: We compared serum proteins from 65 pituitary adenoma patients and 90 healthy donors using proteomic fingerprint technology combining magnetic beads with matrix assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF-MS). RESULTS: A total of 42 M/Z peaks were identified as related to pituitary adenoma (P<0.01). A diagnostic model established based on three biomarkers (3382.0, 4601.9, 9191.2) showed that the sensitivity of diagnosing pituitary adenoma was 90.0% and the specificity was 88.3%. The model was further tested by blind analysis showing that the sensitivity was 88.0% and the specificity was 83.3%. CONCLUSIONS: These results suggest that proteomic fingerprint technology can be used to identify pituitary adenoma biomarkers and the model based on three biomarkers (3382.0, 4601.9, 9191.2) provides a powerful and reliable method for diagnosing pituitary adenoma.

The potential involvement of E-cadherin and beta-catenins in meningioma.

OBJECTIVE: To investigate the potential involvements of E-cadherin and beta-catenin in meningioma. METHODS: Immunohistochemistry staining was performed on samples from patients with meningioma. The results were graded according to the positive ratio and intensity of tissue immunoreactivity. The expression of E-cadherin and beta-catenin in meningioma was analyzed by its relationship with WHO2007 grading, invasion, peritumoral edema and postoperative recurrence. RESULTS: The positive rates of E-cadherin in meningioma WHO I, II, III were 92.69%, 33.33% and 0, respectively, (P<0.05); while the positive rates of beta-catenin in meningioma WHO I, II, III were 82.93%, 33.33% and 20.00%, respectively, (P<0.05). The positive rate of E-cadherin in meningioma without invasion (94.12%) was higher than that with invasion (46.67%) (P<0.05). The difference in the positive rate of beta-catenin between meningioma without invasion (88.24%) and meningioma with invasion (33.33%, P<0.05) was also statically significant. The positive rates of E-cadherin in meningioma with peritumoral edema 0, 1, 2, 3 were 93.75%, 85.71%, 60.00% and 0 respectively, (P<0.05); the positive rates of beta-catenin in meningioma with peritumoral edema 0, 1, 2, 3 were 87.50%, 85.71%, 30.00% and 0 respectively, (P<0.01). The positive rates of E- cadherin in meningioma with postoperative recurrence were 33.33%, and the positive rate with postoperative non-recurrence was 90.00% (P<0.01). The positive rates of beta-catenin in meningioma with postoperative recurrence and non-recurrence were 11.11%, 85.00%, respectively (P<0.01). CONCLUSION: The expression levels of E- cadherin and beta-catenin correlated closely to the WHO 2007 grading criteria for meningioma. In atypical or malignant meningioma, the expression levels of E-cadherin and beta-catenin were significantly lower. The expression levels of E- cadherin and beta-catenin were also closely correlated with the invasion status of meningioma, the size of the peritumoral edema and the recurrent probabilities of the meningioma, all in an inverse correlationship. Taken together, the present study provided novel molecular targets in clinical treatments to meningioma.