Erythrolysis occurs in the clot after intracerebral hemorrhage (ICH) and the release of hemoglobin causes brain injury but it is unclear when such lysis occurs. The present study examined early erythrolysis in rats. ICH rats had an intra-caudate injection of 100 µl autologous blood and sham rats had a needle insertion. All rats had T2 and T2* MRI scanning and brains were used for histology and CD163 (a hemoglobin scavenger receptor) and DARPP-32 (a neuronal marker) immunohistochemistry. There was marked heterogeneity within the hematoma on T2* MRI, with a hyper- or isointense core and a hypointense periphery. Hematoxylin and eosin staining in the same animals showed significant erythrolysis in the core with the formation of erythrocyte ghosts. The degree of erythrolysis correlated with the severity of perihematomal neuronal loss. Perihematomal CD163 was increased by day 1 after ICH and may be involved in clearing hemoglobin caused by early hemolysis. Furthermore, ICH resulted in more severe erythrolysis, neuronal loss and perihematomal CD163 upregulation in spontaneously hypertensive rats compared to Wistar Kyoto rats. In conclusions, T2*MRI detectable early erythrolysis occurred in the clot after ICH, and activated CD163. Hypertension is associated with enhanced erythrolysis in the hematoma.

Artificial aquaporins are synthetic molecules that mimic the structure and function of natural aquaporins (AQPs) in cell membranes. The development of artificial aquaporins would provide an alternative strategy for treatment of AQP-related diseases. In this report, an artificial aquaporin has been constructed from an amino-terminated tubular molecule, which operates in a unimolecular mechanism. The artificial channel can work in cell membranes with high water permeability and selectivity rivaling those of AQPs. Importantly, the channel can restore wound healing of the cells that contain function-lost AQPs.

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Background and Purpose To examine the utility of magnetic resonance imaging (MRI) T2* sequences as a measure of iron overload in the brain following intracerebral hemorrhage (ICH). Methods We examined the time course of T2* changes in the brain around intracerebral hemorrhages in a series of patients. We also performed a series of experiments in an animal model of ICH, examining the time course of T2* changes along with correlation of these changes with histological markers of ferric iron deposition. Results We found that T2* changes in the brain occur with increasing intensity and spatial distribution over a three month period. Experimental ICH in the rat model induces similar changes, and these changes correlate tightly with histological markers of ferric iron deposition. Conclusions MRI T2* changes after ICH can be used to measure the degree of iron overload in the brain. The T2* sequence may be useful as a measure of interventions aimed at reducing ICH-related brain injury by reducing iron deposition.

Object-Hypertension is the main cause of spontaneous intracerebral hemorrhages (ICH), but the effects of hypertension on ICH-induced brain injury have not been well studied. In this study, we examined ICH-induced brain injury in spontaneously hypertensive rats (SHR).Methods-This two-part study was performed on 12 weeks old male SHR and Wistar Kyoto (WKY) rats. First, rats received an intracaudate injection of 0.3 units collagenase and hematoma sizes were determined at 24 hours. Second, rats were injected with 100-μL autologous whole blood into the right basal ganglia. Brain edema, neuronal death, ferritin expression, microglia activation, and neurological deficits were examined.Results-Hematoma sizes were the same in SHR and WKY rats 24 hours after collagenase injection. SHR had greater neuronal death and neurological deficits after blood injection. ICH also resulted in higher brain ferritin levels and stronger activation of microglia in SHR. However, perihematomal brain edema was same in the SHR and WKY rats.Conclusion-Moderate chronic hypertension resulted in more severe ICH-induced neuronal death and neurological deficits, but did not exaggerate hematoma enlargement and perihematomal brain edema in the rat ICH models.

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Background Fibrinogen may play an important role in the survival of trauma patients; however, its role in traumatic brain injury (TBI) and its correlation with disease prognosis remain poorly understood. The aims of this study were to determine the incidence of TBI-associated hypofibrinogenemia in patients with TBI and to evaluate the prognostic value of fibrinogen level with respect to mortality and clinical outcomes. Methods A total of 2570 consecutive TBI patients were retrospectively studied. Prognostic evaluations were determined using the Glasgow Outcome Score (GOS) assessment 3 months after injury. The shape of the relationship between fibrinogen level and mortality or outcome was examined using cubic spline functions. Logistic regression analyses were conducted to identify the association between fibrinogen level and 3-month functional outcomes. Results Fibrinogen concentrations < 2 g/L were observed in 992 (38.6%) patients at the time of admission. Multivariate analyses showed that for patients with fibrinogen levels < 2.0 g/L, those levels were an independent prognostic factor for 3-month mortality (odds ratio [OR], 0.91; 95% confidence interval [CI], 0.89–0.93; P < .001). By contrast, for patients with fibrinogen levels < 2.5 g/L, the levels were an independent prognostic factor for favorable outcomes at 3 months (OR, 1.654; 95% CI, 1.186–2.306; P = .003). Similar results were also seen for patients with fibrinogen levels > 3.0 g/L, with the levels being an independent prognostic factor for favorable outcomes at 3 months (OR, 0.771; 95% CI, 0.607–0.979; P = .033). Conclusions Fibrinogen is an independent prognostic factor for clinical outcomes in TBI patients. Maintaining the level of fibrinogen between 2.5 and 3 g/L may improve clinical outcomes in patients with TBI.

The combination of HBME-1 and either CK19 or galectin-3 or HER-2/neu can improve the specificity of the diagnosis of PTC.