Silicon germanium photo-blocking layers for a-IGZO based industrial display

Amorphous indium- gallium-zinc oxide (a-IGZO) has been intensively studied for the application to active matrix flat-panel display because of its superior electrical and optical properties. However, the characteristics of a-IGZO were found to be very sensitive to external circumstance such as light illumination, which dramatically degrades the device performance and stability practically required for display applications. Here, we suggest the use for silicon-germanium (Si-Ge) films grown plasmaenhanced chemical vapour deposition (PECVD) as photo-blocking layers in the a-IGZO thin film transistors (TFTs). The charge mobility and threshold voltage (V-th) of the TFTs depend on the thickness of the Si-Ge films and dielectric buffer layers (SiNX), which were carefully optimized to be similar to 200 nm and similar to 300 nm, respectively. As a result, even after 1,000 s illumination time, the V-th and electron mobility of the TFTs remain unchanged, which was enabled by the photo-blocking effect of the Si-Ge layers for a-IGZO films. Considering the simple fabrication process by PECVD with outstanding scalability, we expect that this method can be widely applied to TFT devices that are sensitive to light illumination.

Protective effects of Scutellaria baicalensis Georgi against hydrogen peroxide-induced DNA damage and apoptosis in HaCaT human skin keratinocytes

Oxidative stress due to excessive accumulation of reactive oxygen species (ROS) is one of the risk factors for the development of several chronic diseases. In this study, we investigated the protective effects of Scutellaria bai- calensis rhizome ethanol extract (SBRE) against oxidative stress-induced cellular damage and elucidated the un- derlying mechanisms in the HaCaT human skin keratinocyte cell line. Our results revealed that treatment with SBRE prior to hydrogen peroxide (H2O2) exposure significantly increased viability of aCaT cells. SBRE also effectively attenuated H2O2-induced comet tail formation and inhibited the H2O2-induced phosphorylation levels of the histone γH2AX, as well as the number of apoptotic bodies and Annexin V-positive cells. In addition, SBRE exhibited scavenging activity against intracellular ROS generation and restored the mitochondrial membrane po- tential loss by H2O2. Moreover, H2O2 enhanced the cleavage of caspase-3 and degradation of poly (ADP-ribose)- polymerase, a typical substrate protein of activated caspase-3, as well as DNA fragmentation; however, these events were almost totally reversed by pretreatment with SBRE. Furthermore, SBRE increased the levels of heme oxygenase-1 (HO-1), which is a potent antioxidant enzyme, associated with the induction of nuclear fac- tor-erythroid 2-related factor 2 (Nrf2). According to our data, SBRE is able to protect HaCaT cells from H2O2- induced DNA damage and apoptosis through blocking cellular damage related to oxidative stress through a mech-anism that would affect ROS elimination and activating the Nrf2/HO-1 signaling pathway

Sensitization rates of airborne pollen and mold in children

PurposeAeroallergens are important causative factors of allergic diseases. Previous studies on aeroallergen sensitization rates investigated patients groups that had visited pediatric allergy clinics. In contrast, we investigated sensitization rates in a general population group of elementary school to teenage students in Incheon, Jeju, and Ulsan.MethodsAfter obtaining parental consent, skin-prick tests were performed on 5,094 students between March and June 2010. Elementary school students were tested for 18 common aeroallergens, whereas middle and high school students were tested for 25 allergens. The 25 allergens included Dermatophagoides pteronyssinus, Dermatophagoides farinae, pollen (birch, alder, oak, Japanese cedar, pine, willow, elm, maple, Bermuda grass, timothy grass, rye grass, orchard grass, meadow grass, vernal grass, mugwort, Japanese hop, fat hen, ragweed, and plantain), and mold (Penicillatum, Aspergillus, Cladosporium, and Alternaria).ResultsThe sensitization rates in descending order were 25.79% (D. pteronyssinus), 18.66% (D. farinae), 6.20% (mugwort), and 4.07% (willow) in Incheon; 33.35% (D. pteronyssinus), 24.78% (D. farinae), 15.36% (Japanese cedar), and 7.33% (Alternaria) in Jeju; and 32.79% (D. pteronyssinus), 30.27% (D. farinae), 10.13% (alder), and 8.68% (birch) in Ulsan. The dust mite allergen showed the highest sensitization rate among the 3 regions. The sensitization rate of tree pollen was the highest in Ulsan, whereas that of Alternaria was the highest in Jeju. The ragweed sensitization rates were 0.99% in Incheon, 1.07% in Jeju, and 0.81% in Ulsan.ConclusionThe differences in sensitization rates were because of different regional environmental conditions and distinct surrounding biological species. Hence, subsequent nationwide studies are required

Duodenal Mucosa-Associated Lymphoid Tissue Lymphoma: A Case Report

Primary duodenal mucosa associated lymphoid tissue (MALT) lymphoma is very rare, and little is known about its clinical course or effective treatment. We describe a case of primary duodenal MALT lymphoma that was resistant to Helicobacter pylori (H. pylori) eradication and regressed after chemotherapy with cyclophosphamide, vincristine, and prednisolone (CVP). A 71-year-old woman was referred to our department because of epigastric pain and dyspepsia. Gastroduodenoscopy revealed an irregular mucosal nodular lesion with ulceration extending from the bulb to the second portion of the duodenum. Histopathological examination of a biopsy specimen disclosed low-grade MALT lymphoma composed of atypical lymphoid cells with lymphoepithelial lesion. Abdominal CT scans revealed 0.5 to 1.5 cm lymph nodes in the peritoneal cavity, suggestive of lymph node metastasis. We successfully eradicated H. pylori but did not see signs of remission. We administered systemic CVP chemotherapy every 3 weeks. After 6 courses of CVP, the patient achieved complete remission and was followed up without recurrence for about a year

Chlorin e6 Prevents ADP-Induced Platelet Aggregation by Decreasing PI3K-Akt Phosphorylation and Promoting cAMP Production

A number of reagents that prevent thrombosis have been developed but were found to have serious side effects. Therefore, we sought to identify complementary and alternative medicinal materials that are safe and have long-term efficacy. In the present studies, we have assessed the ability of chlorine e6 (CE6) to inhibit ADP-induced aggregation of rat platelets and elucidated the underlying mechanism. CE6 inhibited platelet aggregation induced by 10 µM ADP in a concentration-dependent manner and decreased intracellular calcium mobilization and granule secretion (i.e., ATP and serotonin release). Western blotting revealed that CE6 strongly inhibited the phosphorylations of PI3K, Akt, c-Jun N-terminal kinase (JNK), and different mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase 1/2 (ERK1/2) as well as p38-MAPK. Our study also demonstrated that CE6 significantly elevated intracellular cAMP levels and decreased thromboxane A2 formation in a concentration-dependent manner. Furthermore, we determined that CE6 initiated the activation of PKA, an effector of cAMP. Taken together, our findings indicate that CE6 may inhibit ADP-induced platelet activation by elevating cAMP levels and suppressing PI3K/Akt activity. Finally, these results suggest that CE6 could be developed as therapeutic agent that helps prevent thrombosis and ischemia

Recessive C10orf2 mutations in a family with infantile-onset spinocerebellar ataxia, sensorimotor polyneuropathy, and myopathy

Recessive mutations in chromosome 10 open reading frame 2 (C10orf2) are relevant in infantile-onset spinocerebellar ataxia (IOSCA). In this study, we investigated the causative mutation in a Korean family with combined phenotypes of IOSCA, sensorimotor polyneuropathy, and myopathy. We investigated recessive mutations in a Korean family with two individuals affected by IOSCA. Causative mutations were investigated using whole exome sequencing. Electrophysiological analyses and muscle and nerve biopsies were performed, along with magnetic resonance imaging (MRI) of the brain and lower extremities. Compound heterozygous mutations c.1460C>T and c.1485-1G>A in C10orf2 were identified as causative of IOSCA. Skeletal muscle showed mitochondrial DNA (mtDNA) deletions. Both patients showed a period of normal development until 12–15 months, followed by ataxia, athetosis, hearing loss, and intellectual disability. Electrophysiological findings indicated motor and sensory polyneuropathies. Muscle biopsy revealed variations in the size and shape of myofibers with scattered, small, and angulated degenerating myofibers containing abnormal mitochondria; these observations are consistent with myopathy and may be the result of mtDNA deletions. Sural nerve biopsy revealed an axonal neuropathy. High-signal-intensity lesions in the middle cerebellar peduncles were correlated with clinical severity, and MRI of the lower legs was compatible with the hypothesis of length-dependent axonal degeneration. We identified novel compound heterozygous mutations of the C10orf2 gene as the cause of IOSCA with sensorimotor polyneuropathy and myopathy. Signs of motor neuropathy and myopathy were discovered for the first time in IOSCA patients with C10orf2 mutations. These results suggest that the clinical spectrum of IOSCA caused by C10orf2 mutations may be more variable than previously reported. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10048-014-0405-1) contains supplementary material, which is available to authorized users