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A silicon photonic waveguide switch using adiabatic couplers with lateral comb-drive actuators is designed, fabricated, and tested for microelectromechanical optical matrix switch. One of the waveguides of the adiabatic coupler is moved laterally by three actuators for varying the coupler gap, which enables to switch the path of the waveguides. The coupler waveguides with 250 nm thickness consist of a movable tapered waveguide from 400 nm to 500 nm in width and 50 µm in length and a straight waveguide of 400 nm in width. The three actuators are ultra-small electrostatic comb-drive and move the two movable tapered waveguides. The switch's transmission characteristics were measured as a function of the coupler gap. Around a coupler gap of 109 nm, the port isolation of 16.7 dB was obtained. The switch's insertion loss was roughly estimated to be less than 1 dB. The switching time was 36.7 µsec under the present experimental condition. Moreover, 64 switches were arrayed in a 125 µm period square mash waveguide and an 8 x 8 matrix switch was composed. The matrix switch was also tested.

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Lissencephaly is one of the central nervous system anomalies of Miller-Dieker Syndrome (MDS). Fetuses with lissencephaly have an abnormal smooth brain with fewer folds and grooves that will be detected by ultrasounds or fetal magnetic resonance imaging (MRI) after 30 weeks of gestation. We report a fetus with lissencephaly diagnosed as Miller-Dieker Syndrome postnatally. G banded chromosome analysis revealed 45,X,psu dic(17;Y)(p13;p11.32).ish dic (17;Y)(LIS1-,RARA+, SRY+, DYZ3+) by G-banding analysis using high resolution banding technique. Fetal delayed cortical development will be the findings to perform further investigations including fluorescence in situ hybridization analysis for MDS, a 17p13.3 microdeletion syndrome, pre/postnatally. This will be the first case of MDS with unbalanced translocation between deleted short arm of chromosome 17 and Y chromosome.

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A 40s-year-old woman with previous history of injury due to contact with crown-of-thorns starfish, Acanthaster planci, was stung on the right middle finger. After immediately losing consciousness, she died 13 h after injury despite intensive medical treatment. Examination of the respiratory system revealed narrowing due to severe edema of the laryngopharynx, as well as alveolar hemorrhage, eosinophilic infiltration, and extensive neutrophil and eosinophil aggregation in the intravascular lumen of the lungs. Examination of the liver revealed severe diffuse hepatocellular necrosis and extremely high levels of liver transaminases, indicating severe liver damage. Based on these findings, we concluded that she had died from anaphylactic shock induced by circulation of crown-of-thorns starfish venom in the bloodstream. Injurious contact with the spine of the crown-of-thorns starfish can cause severe symptoms as well as systematic reactions, including anaphylaxis. To our knowledge, this is the first case of anaphylactic shock or death caused by human contact with the crown-of-thorns starfish reported in the English-language literature. Although rare, anaphylaxis due to injury by marine animals is potentially fatal. Saving lives requires providing education regarding prevention and enabling prompt response to possible anaphylaxis, including preparation of adrenaline for auto-injection.

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Here, we describe a high-performance liquid chromatography/photodiode array detector method for the detection of imidacloprid in biological fluids in a case of suicide by ingestion of liquor mixed with Admire® Flowable insecticide (containing 20% imidacloprid). A plastic bottle containing a cloudy liquid (concentration of ethanol in the liquid was 150 mg/ml and that of imidacloprid was 50 mg/ml) was found near the decedent. The biological fluids collected at autopsy were prepared by deproteinization with acetonitrile. Zolpidem was used as an internal standard. The concentrations of imidacloprid in femoral blood and cerebrospinal fluid were 105 and 58.5 µg/ml, respectively. Ethanol was also detected in the samples, with concentrations of 1.0 mg/ml in femoral blood and 1.4 mg/ml in cerebrospinal fluid.

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A 77-year-old man underwent percutaneous transhepatic gallbladder drainage (PTGBD) for acute cholecystitis as a preoperative procedure; however, he suddenly suffered cardiopulmonary arrest 4 h after the PTGBD and died. There were three centesis scars for the PTGBD, and only one pathway from the most dorsal centesis scar reached the gallbladder. Microscopically, the PTGBD pathway crossed and injured the intrahepatic arterial wall, and hepatic parenchymal bleeding extended along the PTGBD pathway to the inferior surface of the liver. Blood flowed to the peritoneal cavity through a small gap between the liver and gallbladder. Consequently, the PTGBD caused lethal bleeding. When the percutaneous transhepatic cholangio drainage/PTGBD pathway runs close to vessels near the liver surface, it might be necessary to deal with the possibility of rapid and lethal peritoneal bleeding.

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A 48-year-old man died from a transnasal intracranial stab wound caused by an umbrella. The track of the stab passed from the right nostril, through the sphenoid sinus, the left side of the sella turcica and anterior clinoid process, and finally reached the surface of the brain. The stab wound crossed the left internal carotid artery, causing an exsanguination and aspiration of blood into the airway, resulting in death. It is extremely rare that an umbrella tip used during a struggle would stab the nostril of the victim. Transnasal intracranial stab wounds can be overlooked and require sensitive handling.

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Although some previous studies have reported patients who developed compartment syndrome or died because of locally applied negative pressure, no detailed investigation of pathologic changes caused by negative pressure-induced injury has been reported in the literature. The main purpose of this study was to examine the morphologic characteristics of injury caused by local negative pressure and correlate these with systemic changes. A total of 30 male Wister rats were used. Animals were randomly assigned to 6 groups. Negative pressure was applied to the right hindlimb of each animal in each group for periods of 0 (sham-operated), 30, 60, 90, 120, or 180 min using a vacuum pump. Macroscopic and microscopic changes induced by local negative pressure were already observed after 30 min and were exacerbated with time. The proportion of muscle degeneration was highest in the deep tissues, irrespective of exposure time. The observed increase in the weight of the injured hindlimb at 180 min was caused by an approximately 30% fluid shift to the hindlimb, demonstrating that the application of negative pressure to the hindlimb of rats can induce hypovolemic shock. We here reveal the morphologic changes induced by local negative pressure and discuss possible mechanisms of negative pressure-induced injury.

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