Spacecraft sample collection and subsurface excavation of asteroid (101955) Bennu.

Carbonaceous asteroids, such as (101955) Bennu, preserve material from the early Solar System, including volatile compounds and organic molecules. We report spacecraft imaging and spectral data collected during and after retrieval of a sample from Bennu's surface. The sampling event mobilized rocks and dust into a debris plume, excavating a 9-meter-long elliptical crater. This exposed material is darker, spectrally redder, and more abundant in fine particulates than the original surface. The bulk density of the displaced subsurface material was 500 to 700 kilograms per cubic meter, which is about half that of the whole asteroid. Particulates that landed on instrument optics spectrally resemble aqueously altered carbonaceous meteorites. The spacecraft stored 250 ± 101 grams of material, which will be delivered to Earth in 2023.

Variations in color and reflectance on the surface of asteroid (101955) Bennu.

Visible-wavelength color and reflectance provide information about the geologic history of planetary surfaces. Here we present multispectral images (0.44 to 0.89 micrometers) of near-Earth asteroid (101955) Bennu. The surface has variable colors overlain on a moderately blue global terrain. Two primary boulder types are distinguishable by their reflectance and texture. Space weathering of Bennu surface materials does not simply progress from red to blue (or vice versa). Instead, freshly exposed, redder surfaces initially brighten in the near-ultraviolet region (i.e., become bluer at shorter wavelengths), then brighten in the visible to near-infrared region, leading to Bennu's moderately blue average color. Craters indicate that the time scale of these color changes is ~105 years. We attribute the reflectance and color variation to a combination of primordial heterogeneity and varying exposure ages.

Episodes of particle ejection from the surface of the active asteroid (101955) Bennu.

Active asteroids are those that show evidence of ongoing mass loss. We report repeated instances of particle ejection from the surface of (101955) Bennu, demonstrating that it is an active asteroid. The ejection events were imaged by the OSIRIS-REx (Origins, Spectral Interpretation, Resource Identification, and Security-Regolith Explorer) spacecraft. For the three largest observed events, we estimated the ejected particle velocities and sizes, event times, source regions, and energies. We also determined the trajectories and photometric properties of several gravitationally bound particles that orbited temporarily in the Bennu environment. We consider multiple hypotheses for the mechanisms that lead to particle ejection for the largest events, including rotational disruption, electrostatic lofting, ice sublimation, phyllosilicate dehydration, meteoroid impacts, thermal stress fracturing, and secondary impacts.

The unexpected surface of asteroid (101955) Bennu.

NASA'S Origins, Spectral Interpretation, Resource Identification and Security-Regolith Explorer (OSIRIS-REx) spacecraft recently arrived at the near-Earth asteroid (101955) Bennu, a primitive body that represents the objects that may have brought prebiotic molecules and volatiles such as water to Earth1. Bennu is a low-albedo B-type asteroid2 that has been linked to organic-rich hydrated carbonaceous chondrites3. Such meteorites are altered by ejection from their parent body and contaminated by atmospheric entry and terrestrial microbes. Therefore, the primary mission objective is to return a sample of Bennu to Earth that is pristine-that is, not affected by these processes4. The OSIRIS-REx spacecraft carries a sophisticated suite of instruments to characterize Bennu's global properties, support the selection of a sampling site and document that site at a sub-centimetre scale5-11. Here we consider early OSIRIS-REx observations of Bennu to understand how the asteroid's properties compare to pre-encounter expectations and to assess the prospects for sample return. The bulk composition of Bennu appears to be hydrated and volatile-rich, as expected. However, in contrast to pre-encounter modelling of Bennu's thermal inertia12 and radar polarization ratios13-which indicated a generally smooth surface covered by centimetre-scale particles-resolved imaging reveals an unexpected surficial diversity. The albedo, texture, particle size and roughness are beyond the spacecraft design specifications. On the basis of our pre-encounter knowledge, we developed a sampling strategy to target 50-metre-diameter patches of loose regolith with grain sizes smaller than two centimetres4. We observe only a small number of apparently hazard-free regions, of the order of 5 to 20 metres in extent, the sampling of which poses a substantial challenge to mission success.

Seizures after decompressive hemicraniectomy for ischaemic stroke.

OBJECTIVE: The risk of seizures after malignant middle cerebral artery (MCA) infarction with decompressive hemicraniectomy (DHC) is uncertain. Also unknown is how this complication influences survivors' recovery and quality of life. METHODS: We retrospectively reviewed medical charts of all patients admitted to Harborview Medical Center between 1 January 2002 and 31 June 2011 for space-occupying MCA ischaemic stroke and who underwent DHC. Survivors and their surrogates were invited to participate in a telephone or in-person interview. RESULTS: Fifty-five patients were followed for a median of 311 days (IQR 134-727). Twenty-seven patients (49%) had seizures, 25 (45%) developed epilepsy and 21 (38%) achieved moderate disability or better (modified Rankin Scale score ≤3) by 1 year after stroke onset. The only factor significantly associated with seizure occurrence was male gender. Median time from stroke to first seizure was 222 days, with a cluster of first seizures within weeks after cranioplasty; only two of the first seizures occurred right around the time of stroke onset. Follow-up time was significantly longer for patients with seizures (605 days, IQR 297-882) than for those without (221 days, IQR 104-335). Of the 20 patients interviewed, 12 achieved moderate disability or better, 15 experienced a seizure with 6 indicating the seizure was a major drawback. Regardless, all 20 would have chosen DHC again. CONCLUSIONS: In this case series, patients were at high risk of developing seizures after malignant MCA stroke with DHC, especially after cranioplasty. Assuming these findings are replicated, means should be sought to reduce the occurrence of this complication.

Immunological consequences of ischemic stroke.

The treatment of ischemic stroke is one of the great challenges in modern neurology. The localization and the size of the infarct determine the long-term disability of stroke survivors. Recent observations have revealed that stroke also alters the function of the immune system and vice versa: At the site of the infarct, a local inflammatory response develops that enhances brain lesion development. In experimental stroke, proof-of-concept studies confirm that inhibition of this immune response reduces lesion volume and improves outcome. In the peripheral blood of stroke patients, though, lymphocytopenia and monocyte dysfunction develop. These changes reflect a clinically relevant impairment of bacterial defense mechanisms because they are associated with an enhanced risk to acquire post-stroke infections. Stress hormones have been identified as important mediators of stroke-induced immune suppression. The pharmacological inhibition of beta adrenergic receptors, but not the inhibition of steroids, is effective in reducing infection and improving clinical outcome in experimental stroke; catecholamine release therefore appears causally related to stroke-induced immune suppression. Strong evidence supports the hypothesis that these immune alterations impact the clinical course of stroke patients. Thus, the development of new therapeutic strategies targeted to alter the immunological consequences of stroke appears promising. However, to date, the beneficial effects seen in experimental stroke have not been successfully translated into a clinical trial. This brief review summarizes the current understanding of the immunological consequences of ischemic stroke. Finally, we propose a concept that links the peripheral immune suppression with the development of local inflammation.

Sensitization and tolerization to brain antigens in stroke.

Despite encounter of novel brain antigens by the systemic immune system following stroke, autoimmune responses to these antigens do not seem to occur. In rats, a systemic inflammatory response at the time of stroke, however, provokes changes that increase the likelihood of developing detrimental autoimmunity. These findings may help to explain why infections in the post-stroke period are associated with worse outcome. In addition, data suggest that the immune response can be manipulated in an antigen specific fashion to improve stroke outcome. Together these data argue that the nature of the post-ischemic immune response influences neurological recovery from stroke.

Intra-arterial urokinase for acute ischemic stroke: factors associated with complications.

The authors abstracted the records of 43 patients treated with intra-arterial urokinase for acute ischemic stroke to identify predictors of serious complications. Sixteen (37%) had such a complication. Higher urokinase dose (>1.5 x 10(6) U), higher mean arterial blood pressure before treatment (>130 mm Hg), basilar occlusive strokes, and severe strokes were most predictive of these complications. Although urokinase is no longer manufactured, these findings identify patients at risk for complications from other intra-arterial thrombolytics.

Targeting the central nervous system inflammatory response in ischemic stroke.

In experimental models of stroke, inflammation appears to contribute to cerebral ischemic injury. Clinical trials that are aimed at limiting the postischemic inflammatory response, however, have thus far had disappointing results. These clinical failures probably reflect the fact that there has been insufficient preclinical data and inadequate trial design, rather than provide evidence against a role for inflammation in ischemic brain injury.

Withdrawal of support in intracerebral hemorrhage may lead to self-fulfilling prophecies.

BACKGROUND: Withdrawal of support in patients with severe brain injury invariably leads to death. Preconceived notions about futility of care in patients with intracerebral hemorrhage (ICH) may prompt withdrawal of support, and modeling outcome in patient populations in whom withdrawal of support occurs may lead to self-fulfilling prophecies. METHODS: Subjects included consecutive patients with supratentorial ICH. Radiographic characteristics of the hemorrhage, clinical variables, and neurologic outcome were assessed. Attitudes about futility of care were examined among members of the departments of neurology and neurologic surgery through a written survey and case presentations. RESULTS: There were 87 patients with supratentorial ICH; overall mortality was 34.5% (30/87). Mortality was 66.7% (18/27) in patients with Glasgow Coma Score < or = 8 and ICH volume > 60 cm(3). Medical support was withdrawn in 76.7% (23/30) of patients who died. Inclusion of a variable to account for the withdrawal of support in a model predicting outcome negated the predictive value of all other variables. Patients undergoing surgical decompression were unlikely to have support withdrawn, and surgery was less likely to be performed in older patients (p < 0.01) and patients with left hemispheric hemorrhage (p = 0.04). Survey results suggested that practitioners tend to be overly pessimistic in prognosticating outcome based upon data available at the time of presentation. CONCLUSIONS: The most important prognostic variable in determining outcome after ICH is the level of medical support provided. Withdrawal of support in patients felt likely to have a "poor outcome" biases predictive models and leads to self-fulfilling prophecies. Our data show that individual patients in traditionally "poor outcome" categories can have a reasonable neurologic outcome when treated aggressively.

Thrombolysis for acute ischemic stroke.

Data generated from randomized controlled trials in the last decade have shown that acute intervention can improve neurologic outcome in patients with ischemic stroke. This article reviews recent studies of systemic and intra-arterial thrombolysis for cerebrovascular disease in detail. Important considerations for treating patients with thrombolysis are explored, and theoretic and practical differences in the approach to patients with anterior and posterior circulation disease are highlighted.

Extravasation of radiographic contrast is an independent predictor of death in primary intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Hematomas that enlarge following presentation with primary intracerebral hemorrhage (ICH) are associated with increased mortality, but the mechanisms of hematoma enlargement are poorly understood. We interpreted the presence of contrast extravasation into the hematoma after CT angiography (CTA) as evidence of ongoing hemorrhage and sought to identify the clinical significance of contrast extravasation as well as factors associated with the risk of extravasation. METHODS: We reviewed the clinical records and radiographic studies of all patients with intracranial hemorrhage undergoing CTA from 1994 to 1997. Only patients with primary ICH were included in this study. Univariate and multivariate logistic regression analyses were performed to determine the associations between clinical and radiological variables and the risk of hospital death or contrast extravasation. RESULTS: Data were available for 113 patients. Contrast extravasation was seen in 46% of patients at the time of CTA, and the presence of contrast extravasation was associated with increased fatality: 63.5% versus 16.4% in patients without extravasation (P=0.011). There was a trend toward a shorter time (median+/-SD) from symptom onset to CTA in patients with extravasation (4.6+/-19 hours) than in patients with no evidence of extravasation (6.6+/-28 hours; P=0.065). Multivariate analysis revealed that hematoma size (P=0.022), Glasgow Coma Scale (GCS) score (P=0.016), extravasation of contrast (P=0.006), infratentorial ICH (P=0.014), and lack of surgery (P<0.001) were independently associated with hospital death. Variables independently associated with contrast extravasation were hematoma size (P=0.024), MABP >120 mm Hg (P=0.012), and GCS score of

Effects of the AMPA receptor antagonist NBQX on outcome of newborn pigs after asphyxic cardiac arrest.

In neonates, asphyxia is a common cause of neuronal injury and often results in seizures. The authors evaluated whether blockade of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors during asphyxia and early recovery with 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo-(F)-quinoxaline (NBQX) ameliorates neurologic deficit and histopathology in 1-week-old piglets. Anesthetized piglets were exposed to a sequence of 30 minutes of hypoxia, 5 minutes of room air ventilation, 7 minutes of airway occlusion, and cardiopulmonary resuscitation. Vehicle or NBQX was administered intravenously before asphyxia (30 mg/kg) and during the first 4 hours of recovery (15 mg/kg/h). Neuropathologic findings were evaluated at 96 hours of recovery by light microscopic and cytochrome oxidase histochemical study. Cardiac arrest occurred at 5 to 6 minutes of airway occlusion, and cardiopulmonary resuscitation restored spontaneous circulation independent of treatment modalities in about 2 to 3 minutes. Neurologic deficit over the 96-hour recovery period was not ameliorated by NBQX. Seizure activity began after 24 to 48 hours in 7 of 10 animals with vehicle and in 9 of 10 of animals with NBQX. In each group, four animals died in status epilepticus. Neuropathologic outcomes were not improved by NBQX. The density of remaining viable neurons was decreased in parietal cortex and putamen by NBQX treatment. Metabolic defects in cytochrome oxidase activity were worsened by NBQX treatment. Seizure activity during recovery was associated with reduced neuronal viability in neocortex and striatum in piglets from both groups that survived for 96 hours. This neonatal model of asphyxic cardiac arrest and resuscitation generates neurologic deficits, clinical seizure activity, and selective damage in regions of basal ganglia and sensorimotor cortex. In contrast to other studies in mature brain, AMPA receptor blockade with NBQX failed to protect against neurologic damage in the immature piglet and worsened postasphyxic histopathologic outcome in neocortex and putamen.

Epidemiology and clinical presentation of aneurysmal subarachnoid hemorrhage.

This article provides an overview of the epidemiology and acquired risk factors associated with intracranial aneurysms and aneurysmal subarachnoid hemorrhage. The clinical presentation of subarachnoid hemorrhage is reviewed and compared to important conditions that can mimic aneurysm rupture, such as thunderclap headache and perimesencephalic nonaneurysmal subarachnoid hemorrhage.

Inflammation and acute stroke.

There are now overwhelming data suggesting that inflammation contributes to cerebral ischemic injury. The mechanisms that lead to the inflammatory response which follows stroke, however, are not fully understood. This review will highlight the most recent advances in our knowledge as well as the early experience of using anti-inflammatory strategies to treat acute stroke.

Immunologic tolerance to myelin basic protein decreases stroke size after transient focal cerebral ischemia.

Immune mechanisms contribute to cerebral ischemic injury. Therapeutic immunosuppressive options are limited due to systemic side effects. We attempted to achieve immunosuppression in the brain through oral tolerance to myelin basic protein (MBP). Lewis rats were fed low-dose bovine MBP or ovalbumin (1 mg, five times) before 3 h of middle cerebral artery occlusion (MCAO). A third group of animals was sensitized to MBP but did not survive the post-stroke period. Infarct size at 24 and 96 h after ischemia was significantly less in tolerized animals. Tolerance to MBP was confirmed in vivo by a decrease in delayed-type hypersensitivity to MBP. Systemic immune responses, characterized in vitro by spleen cell proliferation to Con A, lipopolysaccharide, and MBP, again confirmed antigen-specific immunologic tolerance. Immunohistochemistry revealed transforming growth factor beta1 production by T cells in the brains of tolerized but not control animals. Systemic transforming growth factor beta1 levels were equivalent in both groups. Corticosterone levels 24 h after surgery were elevated in all sham-operated animals and ischemic control animals but not in ischemic tolerized animals. These results demonstrate that antigen-specific modulation of the immune response decreases infarct size after focal cerebral ischemia and that sensitization to the same antigen may actually worsen outcome.

Arterial changes after thrombolysis and percutaneous transluminal angioplasty in vertebrobasilar thrombosis.

We present clinicopathologic findings in a patient treated with intraarterial thrombolysis and angioplasty for vertebrobasilar thrombosis. Autopsy revealed a marked inflammatory infiltrate within the vertebral artery at the site of catheter manipulation. This finding may have important implications for the use of interventional angiography in cerebrovascular disease.

Vertebrobasilar ischemia.

Advances in stroke treatment are discussed in the context of vertebrobasilar ischemia. The anatomy of the vertebral and basilar arteries and the pathophysiology of posterior circulation stroke are reviewed. The diagnosis and management of patients with vertebrobasilar occlusion is emphasized and the controversies surrounding the use of intra-arterial and intravenous thrombolytic therapy in posterior circulation disease are addressed.