BMDCs were cold synchronized with saturating amounts of Ad2 and Ad2-ts1 (60 mg/ml, 0.25 ml per 4610 4 cells on a 12 mm glass coverslip) for 1 h, washed and incubated at 37uC for the indicated times. The samples were fixed with 2.5% glutaraldehyde in 0.1 M ice-cold Na-Cacodylate buffer (pH 7.2) containing 0.5 mg/ml ruthenium red for 1 h, washed with 0.1 M Na-Cacodylate buffer (pH 7.2), post-fixed with 2% OsO4 in the same buffer containing 0.5 mg/ml ruthenium red for 1 h at room temperature, and embedded in Epon as described [105] . Virus particles at the plasma membrane, endosomes and the cytosol were determined, and results expressed as means of analyzed cells (n) with standard errors of the mean. List of accession numbers/ID numbers for proteins mentioned in the text  Hemorrhagic shock and encephalopathy syndrome – the markers for an early HSES diagnosis BACKGROUND: The hemorrhagic shock and encephalopathy syndrome (HSES) is a devastating disease that affects young children. The outcomes of HSES patients are often fatal or manifesting severe neurological sequelae. We reviewed the markers for an early diagnosis of HSES. METHODS: We examined the clinical, biological and radiological findings of 8 patients (4 months to 9 years old) who met the HSES criteria. RESULTS: Although cerebral edema, disseminated intravascular coagulopathy (DIC), and multiple organ failure were seen in all 8 cases during their clinical courses, brain computed tomography (CT) scans showed normal or only slight edema in 5 patients upon admission. All 8 patients had normal platelet counts, and none were in shock. However, they all had severe metabolic acidosis, which persisted even after 3 hours (median base excess (BE), -7.6 mmol/L). And at 6 hours after admission (BE, -5.7 mmol/L) they required mechanical ventilation. Within 12 hours after admission, fluid resuscitation and vasopressor infusion for hypotension was required. Seven of the patients had elevated liver enzymes and creatine kinase (CK) upon admission. Twenty-four hours after admission, all 8 patients needed vasopressor infusion to maintain blood pressure. CONCLUSION: CT scan, platelet count, hemoglobin level and renal function upon admission are not useful for an early diagnosis of HSES. However, the elevated liver enzymes and CK upon admission, hypotension in the early stage after admission with refractory acid-base disturbance to fluid resuscitation and vasopressor infusion are useful markers for an early HSES diagnosis and helpful to indicate starting intensive neurological treatment. Since the original description of the hemorrhagic shock and encephalopathy syndrome (HSES) by Levin et al. [1] , numerous cases have been reported in the literature. Although the etiology of HSES remains unknown, this syndrome is associated with acute onset of encephalopathy, shock, watery diarrhea, severe disseminated intravascular coagulopathy (DIC), and renal and hepatic dysfunction.