Dilated Optic Nerve Sheath Diameter Predicts Poor Outcome in Acute Spontaneous Intracerebral Hemorrhage.

BACKGROUND AND PURPOSE: Optic nerve sheath diameter (ONSD) enlargement occurs in patients with intracerebral hemorrhage (ICH). However, the relationship between ONSD and prognosis of ICH is uncertain. This study aimed to investigate the predictive value of ONSD on poor outcome of patients with acute spontaneous ICH. METHODS: We studied 529 consecutive patients with acute spontaneous ICH who underwent initial CT within 6 h of symptom onset between October 2016 and February 2019. The ONSDs were measured 3 mm behind the eyeball on initial CT images. Poor outcome was defined as having a Glasgow Outcome Scale (GOS) score of 1-3, and favorable outcome was defined as having a GOS score of 4-5 at discharge. RESULTS: The ONSD of the poor outcome group was significantly greater than that of the favorable outcome group (5.87 ± 0.86 vs. 5.21 ± 0.69 mm, p < 0.001). ONSD was related to hematoma volume (r = 0.475, p < 0.001). Adjusting other meaningful predictors, ONSD (OR: 2.83; 95% CI: 1.94-4.15) was associated with poor functional outcome by multivariable logistic regression analysis. Receiver operating characteristic curve showed that the ONSD improved the accuracy of ultraearly hematoma growth in the prediction of poor outcome (AUC: 0.790 vs. 0.755, p = 0.016). The multivariable logistic regression model with all the meaningful predictors showed a better predictive performance than the model without ONSD (AUC: 0.862 vs. 0.831, p = 0.001). CONCLUSIONS: The dilated ONSD measured on initial CT indicated elevated intracranial pressure and poor outcome, so appropriate intervention should be taken in time.

A nomogram to predict rupture risk of middle cerebral artery aneurysm.

BACKGROUND: Determining the rupture risk of unruptured intracranial aneurysm is crucial for treatment strategy. The purpose of this study was to predict the rupture risk of middle cerebral artery (MCA) aneurysms using a machine learning technique. METHODS: We retrospectively reviewed 403 MCA aneurysms and randomly partitioned them into the training and testing datasets with a ratio of 8:2. A generalized linear model with logit link was developed using training dataset to predict the aneurysm rupture risk based on the clinical variables and morphological features manually measured from computed tomography angiography. To facilitate the clinical application, we further constructed an easy-to-use nomogram based on the developed model. RESULTS: Ruptured MCA aneurysm had larger aneurysm size, aneurysm height, perpendicular height, aspect ratio, size ratio, bottleneck factor, and height-width ratio. Presence of a daughter-sac was more common in ruptured than in unruptured MCA aneurysms. Six features, including aneurysm multiplicity, lobulations, size ratio, bottleneck factor, height-width ratio, and aneurysm angle, were adopted in the model after feature selection. The model achieved a relatively good performance with areas under the receiver operating characteristic curves of 0.77 in the training dataset and 0.76 in the testing dataset. The nomogram provided a visual interpretation of our model, and the rupture risk probability of MCA aneurysms can be directly read from it. CONCLUSION: Our model can be used to predict the rupture risk of MCA aneurysm.

Propofol inhibits gap junctions by attenuating sevoflurane-induced cytotoxicity against rat liver cells in vitro.

BACKGROUND: Liver abnormalities are seen in a small proportion of patients following anaesthesia with sevoflurane. OBJECTIVES: To investigate whether the cytotoxicity of sevoflurane against rat liver cells was mediated by gap junction intercellular communications, and the effect of propofol on sevoflurane-induced cytotoxicity. DESIGN: Experimental study. SETTING: The study was carried out in the central laboratory of The Third Affiliated Hospital, Sun Yat-sen University. CELL LINE: BRL-3A rat liver cells. METHODS: Immortal rat liver cells BRL-3A were grown at low and high density. Colony-forming assays were performed to determine clonogenic growth of these cells. To investigate the effect of oleamide and propofol on gap junction function, we measured fluorescence transmission between cells using parachute dye-coupling assays. Immunoblotting assays were performed to determine connexin32 and connexin43 expression. RESULTS: Our colony formation assays revealed that, in low-density culture, sevoflurane caused no apparent inhibition of clonogenic growth of BRL-3A cells. In high-density culture, 2.2 to 4.4% sevoflurane markedly inhibited clonogenic growth of BRL-3A cells with 67.6 (0.34)% and 61.2 (0.17)% of the cells being viable, respectively (P = 0.003 vs. low-density culture), suggesting cell density dependency of sevoflurane-induced cytotoxicity. Our colony formation assays revealed that propofol markedly attenuated the suppression by sevoflurane of the clonogenic growth of BRL-3A cells (viability: propofol and sevoflurane, 91.5 (0.014)% vs. sevoflurane, 56.6 (0.019)%; P <0.01). Blocking gap junctions with 10 µmol l oleamide significantly attenuated 4.4% sevoflurane-induced suppression with a viability of 83.6 ±â€Š0.138% (oleamide and sevoflurane vs. sevoflurane, P < 0.01). Immunoblotting assays further showed that propofol (3.2 µg ml) markedly reduced CX32 levels and significantly inhibited gap junctional intercellular communications as revealed by parachute dye-coupling assays. Values are mean (SD). CONCLUSION: This study provides the first direct evidence that sevoflurane-induced cytotoxicity, which is mediated through gap junctions, is attenuated by propofol, possibly by its action on Cx32 homomeric or heteromeric complexes.

[Effects of cromolyn sodium on intestinal ischemia-reperfusion injury by inhibiting PAR-2 expression in rats].

OBJECTIVE: To explore the effects of cromolyn sodium (CS) on intestinal ischemia-reperfusion (IIR) and its relationship with mast cell activation and protease-activated receptor 2 (PAR-2) expression. METHODS: A total of 32 SD rats were randomly divided into 4 groups: sham-operated (S), intestinal ischemia reperfusion (IIR), CS (a mast cell stabilizer, CS, 25 mg/kg) and compound 48/80 (a mast cell degranulation, CP, 0.75 mg/kg) (n = 8 each). IIR was induced by clamping superior mesenteric artery for 75 min followed by reperfusion for 3 hours. The above agents were intravenously administrated at 5 min pre-reperfusion. Rats were then sacrificed and intestinal issues harvested for histological examinations. The tryptase expression and mast cell count were analyzed by immunohistochemistry. PAR-2 was analyzed by Western blot. RESULTS: The Chiu's score (0.75 ± 0.21), mast cell count (10 ± 3), tryptase expression (125 ± 15) and PAR-2 expression (109 ± 10) of group S were the least while those of group CP the most (all P < 0.05). The Chiu's score (2.14 ± 0.64), mast cell count (15 ± 4), tryptase expression (138 ± 17) and PAR-2 expression (124 ± 12) of group CS were less than those of groups IIR and CP (all P < 0.05). CONCLUSION: Cromolyn sodium may reduce IIR injury by stabilizing mast cell membrane and inhibiting the expressions of tryptase and PAR-2.

Serum vascular endothelial growth factor-C and lymphoangiogenesis are associated with the lymph node metastasis and prognosis of patients with colorectal cancer.

BACKGROUND: The study aims to investigate the relationship among serum vascular endothelial growth factor (SVEGF-C), VEGF-C expression and lymph vessel density (LVD) in tumour tissue, and their influence to colorectal carcinoma (CRC). METHODS: The SVEGF-C concentration of 110 patients with CRC and 40 healthy donors was examined by ELISA. The 110 tumour tissues and 40 normal colorectal specimens were examined by immunohistochemical staining (SP method) with VEGF-C and podoplanin (lymphatic vessel specific antibody). Kaplan­Meier survival analysis determined the influence on CRC prognosis. RESULTS: CRC SVEGF-C level (889.0 ± 264.0 pg/mL) significantly exceeded (P = 0.000) the control level (373.2 ± 97.3 ng/L), and was significantly higher in T3, lymph node metastasis (LNM), distant metastasis, and pTNM groups III and IV. LNM prediction sensitivity, specificity, and accuracy of SVEGF-C were 85.7, 80.0 and 83.6%, respectively (875 pg/mL cut-off). VEGF-C expression was elevated in CRC versus control patients (P = 0.000), and was significantly related to LNM and pTNM stages III and IV. Mean LVD in CRC (6.3 ± 0.7/200 HP) significantly exceeded control mean (3.0 ± 0.7/200 HP) (P = 0.000). LVD was significantly higher in LNM and pTNM stages III and IV. SVEGF-C level was significantly higher in VEGF-C positive versus negative patients (P = 0.000), and was related to LVD (P = 0.009). Kaplan­Meier ranking of prognostic factors was SVEGF-C level (P = 0.000), VEGF-C expression (P = 0.001) and LVD (P = 0.012). CONCLUSION: SVEGF-C level, VEGF-C and LVD are related to LNM and poor prognosis in patients with CRC. SVEGF-C may be a biomarker for LNM in CRC.