The crystalline silicon heterojunction structure adopted in photovoltaic modules commercialized as Panasonic's HIT has significantly reduced recombination loss, resulting in greater conversion efficiency. The structure of an interdigitated back contact was adopted with our crystalline silicon heterojunction solar cells to reduce optical loss from a front grid electrode, a transparent conducting oxide (TCO) layer, and a-Si:H layers as an approach for exceeding the conversion efficiency of 25%. As a result of the improved short-circuit current (J sc ), we achieved the world's highest efficiency of 25.6% for crystalline silicon-based solar cells under 1-sun illumination (designated area: 143.7 cm 2 ).

Glycoconjugate polystyrenes bearing sialyllactose moieties were prepared via a simple method from a mixture of alpha2-6 and a2-3 linked sialyllactose isomers of bovine milk origin. The reducing end of sialyllactose was converted to an amino function with ammonium hydrogen carbonate and then coupled with p-vinylbenzoyl chloride. The resulting styrene derivative substituted with sialyllactose via an amide linkage was polymerized with ammonium peroxodisulfate and N,N,N',N-tetramethylethylenediamine in water at 30 degrees C. The interaction of the glycopolymer with influenza A and B viruses was investigated by three different methods. The glycopolymer inhibited the hemagglutination of influenza A virus (PR/8/34) and its activity was 10(3) times higher than that of the oligosaccharide itself. The cytopathic effect of virus-infected MDCK (Madine-Darby canine kidney) cells was inhibited by the glycopolymer. The homopolymer showed 10(2) times higher inhibitory activity than naturally-occurring fetuin. It was also found that various viruses could be trapped by the glycopolymer adsorbed on a polystyrene surface. The inhibitory and trapping activities of the glycopolymers were correlated with the sialyl linkage specificities of the virus strains.

Dural arteriovenous fistula (DAVF) can be separated into two types: DAVF which drains through an affected sinus (sinus type) and DAVF with direct reflux to the cortical vein (non-sinus type). The present report attempted to clarify the mechanism of formation and development of DAVF focusing on the emissary vein (EV) hypothesis. First, inflammation occurs at the penetrating point of the EV on the dura due to idiopathic or secondary causes. Local inflammatory reactions induce vessel dilatation and neovascularization, and subsequently create arteriovenous (AV) connections on the arteriole level. Although EV communicating with dural arteries might play a role as draining routes at first, they start to degrade due to compression of enlarged emissary arteries or to a hemodynamic shift to the drainage pathway of least resistance. Following the occlusion of drainage pathway through EV into the sinus or cortical veins may form, resulting in clinically detectable DAVF. The AV shunt then expands to the surrounding dura associated with recruitment of feeders from distant sites induced by expression of angiogenetic factors and a shift in the hemodynamic balance. In sinus type DAVF, the sinus is progressively compartmentalized and finally occludes due to thrombogenesis with activated coagulopathy or to hemodynamic hypertrophy of the sinus wall. This progression results in the mature, aggressive DAVF with drainage impairments. Previous mechanistic hypotheses focusing on sinus hypertension and sinus thromboses cannot explain the pathogenesis of non-sinus type of DAVF. Although the etiology of DAVF may be concerned by the thrombo-occlusive change of sinus, the unique theory presented in this report may enable an understanding of the common etiology of both types of DAVF.

Endovascular coil embolization can be considered as an alternative treatment option for selective saccular-shaped BBAs.

The authors retrospectively reviewed their cases of infectious intracranial aneurysms and discuss results and trends of current treatment modalities including medical, neurosurgical, and endovascular. Twenty patients (10 males and 10 females; mean age 46 years) with 23 infectious aneurysms were treated by various treatment modalities during a 15-year period.

Contrast-induced encephalopathy is a very rare complication associated with endovascular treatment of intracranial aneurysms. Patients with renal dysfunction may be prone to developing contrast medium neurotoxicity as a result of delayed elimination of the contrast medium in renal metabolism. This article focuses on our experience with contrast-induced encephalopathy in patients with end-stage renal disease requiring hemodialysis. The authors retrospectively reviewed five patients diagnosed with contrast-induced encephalopathy who underwent aneurysm coil embolization at their institution from January 2006 to December 2015. During the 10-year period, embolization was performed in 755 cases, among which contrast-induced encephalopathy occurred in five patients (0.66%). Three of the five patients were undergoing dialysis for chronic renal failure (one male and two female; mean age 66.7). Embolization for hemodialysis patients was performed in eight during the same period and the incidence of contrast-induced encephalopathy in hemodialysis patients is quite high in our series (3 of 8; 38%). Procedures were performed in one for recurrence of unruptured anterior-communicating artery aneurysm and in two for unruptured basilar-tip aneurysm. Mean approximately 220 ml of contrast media was used among three hemodialysis patients. All three patients showed an improvement or a control in symptoms soon after hemodialysis. Recovery of neurological symptoms was complete in two and almost normal in one within 1 week after intervention. Contrast-induced encephalopathy should be kept in mind as an expected complication of aneurysm embolization in hemodialysis patients. In hemodialysis patients with contrast-induced encephalopathy, performing hemodialysis is an effective treatment to improve symptoms early.

This is the first study suggesting TN-C increases with close linkage to the occurrence of vasospasm after SAH.

Low response to clopidogrel had little effect on clinical outcome although it increased asymptomatic large ischemic lesions in this cohort.