Anti-N-methyl-d-aspartate receptor encephalitis.

Anti-N-methyl-d-aspartate (NMDA) receptor encephalitis is a treatment-responsive encephalitis associated with anti-NMDA receptor antibodies, which bind to the NR1/NR2 heteromers of the NMDA receptors. It is a highly characteristic syndrome evolving in five stages: the prodromal phase (viral infection-like symptoms), psychotic phase, unresponsive phase, hyperkinetic phase, and gradual recovery phase. It has been considered as a paraneoplastic syndrome usually affecting childbearing-age female with ovarian tumors; however, recent reports suggest a much higher incidence of nonparaneoplastic cases in children. We report a 14-year-old girl with anti-NMDA receptor encephalitis without a detectable tumor who showed a nearly complete recovery after intensive immunotherapy.

Congenital chylothorax in a late preterm infant and successful treatment with octreotide.

Chylothorax is defined as abnormal accumulation of lymphatic fluid in the pleural space and is a rare condition in neonates. Chylothorax causes respiratory and nutritional problems and a significant mortality rate. Octreotide is a long-acting somatostatin analog that can reduce lymphatic fluid production and has been used as a new strategy in the treatment of chylothorax. Here, we report a premature baby with severe bilateral pleural effusion diagnosed by prenatal ultrasound and subsequently confirmed to be congenital chylothorax after birth. This newborn baby was initially treated with bilateral chest tube insertion to relieve severe respiratory distress. However, the chylothorax recurred after a medium-chain-triglyceride-enriched formula was initiated. The accumulation of chylothorax diminished after the administration of octreotide. Therefore, octreotide may allow the patient to avoid invasive procedures, such as reinsertion of chest tubes or surgery.

Human umbilical cord blood cells protect against hypothalamic apoptosis and systemic inflammation response during heatstroke in rats.

BACKGROUND: Intravenous administration of human umbilical cord blood cells (HUCBC) has been shown to improve heatstroke by reducing arterial hypotension as well as cerebral ischemia and damage in a rat model. To extend these findings, we assessed both hypothalamic neuronal apoptosis and systemic inflammatory responses in the presence of HUCBCs or vehicle medium immediately after initiation of heatstroke. METHODS: Anesthetized rats, immediately after the initiation of heat stress, were divided into two groups and given either serum-free lymphocyte medium (0.3mL per rat, intravenously) or HUCBCs (5 x 10(6) in 0.3 mL serum-free lymphocyte medium, intravenously). Another group of rats were exposed to room temperature (26 degrees C) and used as normothermic controls. Heatstroke was induced by exposing the anesthetized rats to a high ambient temperature of 43 degrees C for 68 minutes. RESULTS: After the onset of heatstroke, animals treated with serum-free lymphocyte medium displayed hyperthermia, hypotension, bradycardia, hypothalamic neuronal apoptosis and degeneration, and up-regulation of systemic inflammatory response molecules including serum tumor necrosis factor-alpha, soluble intercellular adhesion molecule-1 and E-selectin. Heatstroke-induced hypotension, bradycardia, hypothalamic neuronal apoptosis and degeneration, and increased systemic inflammatory response molecules were significantly inhibited by HUCBC treatment. Although heatstroke-induced hyperthermia was not affected by HUCBC treatment, the serum levels of the anti-inflammatory cytokine interleukin-10 were significantly increased by HUCBC therapy during hyperthermia. CONCLUSIONS: These findings suggest that HUCBC transplantation may prevent the occurrence of heatstroke by reducing hypothalamic neuronal damage and the systemic inflammatory responses.

Infusion of human umbilical cord blood cells ameliorates hind limb dysfunction in experimental spinal cord injury through anti-inflammatory, vasculogenic and neurotrophic mechanisms.

BACKGROUND: Human umbilical cord blood cells (HUCBCs) were used to investigate the mechanisms underlying the beneficial effects of cord blood cells in spinal cord injury (SCI). METHODS: Rats were divided into three groups: (1) sham operation (laminectomy only); (2) Laminectomy+SCI+human adult peripheral blood mononucleocytes (PBMCs) (5 x 10(6)/0.3 mL); and (3) Laminectomy+SCi+HUCBCs (5 x 10(6)/0.3 mL). SCI was induced by compressing the spinal cord for 1 minute with an aneurysm clip calibrated to 55 g closing pressure. HUCBCs were infused immediately after SCI via the tail vein. Behavioral function tests measuring the maximal angle at which an animal could hold onto the inclined plane were conducted on days 1, 4 and 7 after SCI. Serum levels of tumor necrosis factor (TNF)-alpha and interleukin (IL)-10, were assayed. Furthermore, to determine if glial cell line-derived neurotrophic factor (GDNF) or vascular endothelial growth factor (VEGF) could be detected in the spinal cord injured area after systemic HUCBC infusion, analysis of these two molecules was conducted by immunofluorescence. RESULTS: Systemic HUCBC infusion significantly attenuated SCI-induced hind limb dysfunction. The serum IL-10 levels were increased, but TNF-alpha levels were decreased after HUCBC infusion. Both VEGF and GDNF could be detected in the injured spinal cord after transplantation of HUCBC, but not PBMC, cells. CONCLUSION: Our results demonstrate that HUCBC therapy may be beneficial for the recovery of SCI-induced hind limb dysfunction by increasing serum levels of IL-10, VEGF and GDNF in SCI rats.

Disseminated pneumococcal infection with pericarditis and cardiac tamponade: report of one case.

A 1-year-5-months-old female who had cough, rhinorrhea and prolonged fever for 19 days was admitted to the intensive care unit due to exertional dyspnea. She was intubated promptly in virtue of hypotension and cyanosis. The physical examination demonstrated diminished breathing sound over the right lung and distant heart sound; echocardiogram showed cardiac tamponade. Further X ray study showed right hydropneumothorax and cardiomegaly. Pericardiocentesis and chest thoracostomy were performed, and subsequently all the cultures showed growth of Streptococcus pneumoniae. Antibiotics therapy was started promptly after admission. Further investigation indicated osteomyelitis of the right ilium, so that surgical debridement was done. The patient was discharged 54 days later with complete recovery. After following up for 18 months, no restrictive heart disease developed. Purulent pericarditis with cardiac tamponade is an extremely rare complication of pneumococcal infection.