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Fracture hematoma formation describes a transitional phase that involves a dynamic and tightly choreographed interaction between the fibrin matrix, cells, and cytokines that guides the ensuing bone repair. Here we propose a novel hypothesis to explain why hematomas in conjunction with critical sized bone defects are prone to differentiate into fibrous tissues, which eventually results in non-unions of the bone. We postulate that certain hematoma qualities are triggers that influence cell biological behaviours and that the release of certain growth factors determines what pattern of remodelling will prevail: intramembranous or endochondral ossification. A detailed characterization of the structural parameters of hematomas will allow researchers to create a microenvironment that aids the migration of mesenchymal stromal cells into the hematoma where, once established, they accelerate the bone healing process. Such a strategy would be particularly useful when faced with the complications arising from large recalcitrant bone defects that often fail to heal naturally. [ABSTRACT FROM AUTHOR]

Objective Unruptured paraclinoid aneurysms are often asymptomatic, and endovascular coiling is the main treatment. However, endovascular treatment of these lesions still leads to neurologic complications. We aimed to identify predictors of neurologic complications in these lesions. Methods We retrospectively analyzed patients with unruptured paraclinoid aneurysms who were treated with endovascular coiling between January 2014 and December 2015. A neurologic complication was defined as any transient or permanent increase in the modified Rankin Scale score after aneurysm embolization. Univariate and mulitivariate logistic regression analyses were performed to assess the risk factors of neurologic complications. Results Of the 443 unruptured paraclinoid aneurysms that were included in this study, the incidence of neurologic complications was 5.2%. Neurologic complications were highly correlated with hypertension (odds ratio [OR], 3.147; 95% confidence interval [CI], 1.217–8.138; P = 0.018), cerebral ischemic comorbidities (OR, 3.396; 95% CI, 1.378–8.374; P = 0.008), and aneurysm size (OR, 7.714; 95% CI, 1.784–31.635; P < 0.001), and irregular shape (OR, 3.157; 95% CI, 1.239–8.043; P = 0.016) in the univariate analysis. Cerebral ischemic comorbidities (OR, 2.837, 95% CI, 1.070–7.523; P = 0.036) and aneurysm size as dichotomous variables (OR, 7.557; 95% CI, 2.975–19.198; P < 0.001) were strongly correlated with neurologic complications in the final adjusted multivariate logistic analysis. Conclusions Unruptured paraclinoid aneurysms after endovascular treatments had 5.2% of neurologic complications. Cerebral ischemic comorbidities and aneurysm size were predictors of neurologic complications. [ABSTRACT FROM AUTHOR]

Background and Objective Patients with small (<5 mm) unruptured intracranial aneurysms (UIAs) are at risk of subarachnoid hemorrhage, but risk assessment of these patients remains controversial in daily clinical practice. We aimed to identify the risk factors of aneurysmal rupture in these patients. Methods We retrospectively analyzed consecutive patients with small UIAs who were admitted to our center between February 2009 and December 2014. The enrolled patients were divided into ruptured and unruptured groups. The risk factors for aneurysmal rupture were determined using multivariate logistic regression analysis. Results A total of 548 patients with 618 small intracranial aneurysms (267 ruptured and 351 unruptured) were included. Univariate analysis showed that rupture of small aneurysms was related to sex, age, smoking, hypertension, aspect ratio, size ratio, irregular shape, aneurysm width, height, and neck diameter, and location at bifurcation or posterior circulation. Multivariate logistic regression showed that rupture was associated with bifurcation location (odds ratio [OR], 5.409; 95% confidence interval [CI], 3.656–8.001; P < 0.001), size ratio (OR, 3.092; 95% CI, 2.002–4.774; P < 0.001), location (OR, 2.624; 95% CI, 1.428–4.824; P = 0.002), hypertension (OR, 1.698; 95% CI, 1.1140–2.527; P = 0.009), and age at diagnosis of UIA (OR, 1.826; 95% CI, 1.225–2.723; P = 0.003). Conclusions This study showed that 70.4% of small ruptured intracranial aneurysms (<5 mm) were located at parent artery bifurcations and that bifurcation location was a significant independent factor for the risk of rupture of small UIAs (<5 mm). Prophylactic treatment should be recommended for small UIAs in this location. [ABSTRACT FROM AUTHOR]

An important therapeutic method of glioblastoma, the most common primary brain tumor, is radiotherapy. However, several studies reported recently that radiation could also promote the invasion and migration of malignant tumor. Herein, we have identified that a significant increase of migration and invasiveness of human glioma U251 cells undergoing X-ray was observed compared to controls, accompanied by the increase of cathepsin L (CTSL), which is a lysosomal cysteine protease overexpressed and secreted by tumor cells. To verify if there was a relationship between CTSL and the X-ray-induced glioma invasion, a CTSL specific inhibitor Z -FY-CHO or a short hairpin RNA interference was used to pretreat U251 cells. As a result, the cell invasion and migration was impaired via down-regulation of CTSL. Additionally, a marked reduction of the cell-signaling molecules Rho kinase was also detected compared with controls. We also found that CTSL is involved in EMT progress: both in vitro and in clinical specimens. Overall, our findings show that CTSL is an important protein which mediates cell invasion and migration of human glioma U251 cells induced by X-ray, and the inhibition of CTSL expression might diminish the invasion of U251 cells by reducing the activity of RhoA and CDC42 as well as EMT positive markers. [ABSTRACT FROM AUTHOR]

Dysregulated microRNAs (miRNAs) have been reported to involve in the pathophysiological process of traumatic brain injury (TBI), and modulate autophagy-related genes (ATGs) expression. Our previous studies showed that neuronal autophagy was activated in the injury hippocampus post- TBI and associated with neurological and cognitive impairments. The present study was designed to investigate the possible role of miR-23b in TBI-induced cognitive impairments. We found the overexpression of miR-23b conferred a better neuronprotective effects after TBI by decreasing lesion volume, alleviating brain edema, inhibiting neuron apoptosis and attenuating long-term neurological deficits, and most interestingly, improving cognitive impairments. To further explore the molecular underlying this neuronprotection, we evaluated autophagic activity and ATG12 expression in the injury hippocampus CA1 region. The results identified that miR-23b directly targeted to the 3′UTR region of ATG12 mRNA to suppress the activation of neuronal autophagy by a dual-luciferase reporter system. Notably, overexpression of ATG12 abrogated the neuronprotective effects of miR-23b on TBI-induced neurological and cognitive impairments. Taken together, these date revealed inhibition of ATG12-mediated autophagic activity by miR-23b overexpression might be involve in cognitive improvement after TBI, indicating that miR-23b might be a potential therapeutic target for TBI. [ABSTRACT FROM AUTHOR]