Surface treatment of flow channels in microfluidic devices fabricated by stereolithography.

A microfluidic device with three-dimensional flow channels was fabricated by stereolithography, and hydrophilic surface treatment of the flow channel was performed by coating the wall of the channel with a silica layer. After the treatment, the device produced monodisperse oil-in-water (O/W) emulsions. The silica layer on the channel surface was then coated with a fluorinated silane coupling agent to make it hydrophobic, thus enabling the treated device to produce monodisperse inverted water-in-oil (W/O) emulsions.

[A case of coil embolization for unexpected massive bleeding caused by internal carotid artery injury].

We experienced a case of coil embolization for unexpected massive bleeding due to the injury of the internal carotid artery during surgery. A 78-year-old woman underwent right maxillectomy for a malignant tumor in the maxilla. Three hours after the start of the operation, uncontrollable bleeding occurred suddenly, with the blood loss reaching 4,600 ml in 10 minutes. Blood pressure decreased precipitously, but systolic blood pressure recovered to 90 mmHg after rapid infusion and transfusion. The bleeding point could not be identified, and hemostasis by gauze compression was tried in vain. After a large amount of fluid replacement in a short period, the hemoglobin concentration decreased to 2.5 g x dl(-1) temporarily. Angiography revealed the injury of the right internal carotid artery. Coil embolization in the internal carotid artery was performed unilaterally for hemostasis. The total blood loss amounted to 28 liters, and the patient received 2,000 ml of albumin solution, 68 units of red cell concentrates and 50 units of fresh frozen plasma in addition to 18,420 ml of lactated Ringer solution. Operation time was 17 hours and 48 minutes. Despite unexpected massive bleeding and hemodilution, maxillectomy was completed and the patient recovered without any postoperative sequelae.

Effects of propofol and pentobarbital on calcium concentration in presynaptic boutons on a rat hippocampal neuron.

PURPOSE: Numerous reports suggest that intravenously administered (IV) anesthetics affect postsynaptic events in the central nervous system. However, there is little evidence about how general anesthetics influence the presynaptic processes. The level of presynaptic calcium (Ca(2+)) concentration ([Ca(2+)](pre)) regulates neurotransmitter release. In this study, we investigated the effects of anesthetic propofol IV and the barbiturate pentobarbital on neurotransmitter release by measuring [Ca(2+)](pre) in the presynaptic nerve terminals (boutons) on a dissociated single hippocampal rat neuron. METHODS: Sprague-Dawley rats 10-14 days old were decapitated under pentobarbital anesthesia, and brain slices were prepared. The hippocampal CA1 area was touched with a fire-polished glass pipette, which vibrated horizontally, and neurons were dissociated, along with the attached presynaptic boutons. The presynaptic boutons were visualized under a confocal laser-scanning microscope after staining with FM1-43 dye, and [Ca(2+)](pre) was measured with acetoxymethyl ester of fluo-3 (fluo-3 AM). RESULTS: High potassium (K(+)) (15-90 mM) increased the [Ca(2+)](pre) in the Ca(2+)-containing solution in a concentration-dependent manner. Whereas propofol (10 µM) and pentobarbital (300 µM) suppressed the high K(+) (60 mM)-induced increase in [Ca(2+)](pre) in the boutons attached to the dendrite, they did not affect [Ca(2+)](pre) in the boutons attached to the soma or dendrite base. As a large majority of excitatory synapses are located on dendritic spines, these agents may affect Ca(2+) mobilization in the excitatory presynaptic boutons. CONCLUSIONS: Propofol and pentobarbital may affect neurotransmitter release from the excitatory presynaptic nerve terminals due to inhibition of increase in [Ca(2+)](pre).