Enhancement of the efficiency in p-i-n organic light-emitting devices containing organic p-type HAT-CN and n-type bis(ethylenedithio)- tetrathiafulvalene doped BPhen layers.

The p-i-n organic light-emitting devices (OLEDs) were fabricated by using a p-type 1,4,5,8,9,11-hexaazatriphenylene hexacarbonitrile (HAT-CN) layer and an n-type bis(ethylenedithio)-tetrathiafulvalene (BEDT-TTF) doped 4,7-diphenyl-1,10-phenanthroline (BPhen) electron transport layer. The p-i-n OLEDs containing a p-type HAT-CN layer and BEDT-TTF-doped BPhen layer with a BEDT-TTF doping concentration of 1 wt.% demonstrated low operating voltage and the highest luminance efficiency. The enhancement of the luminance efficiency as well as a decrease in the operating voltage of the OLEDs was attributed to the improvement of the hole and electron injection due to the insertion of a HAT-CN layer and a BEDT-TTF-doped BPhen layer.

Three novel mutations of the PKD1 gene in Korean patients with autosomal dominant polycystic kidney disease.

Mutations at the PKD1 locus account for 85% of cases of the common genetic disorder called autosomal dominant polycystic kidney disease (ADPKD). Screening for mutations of the PKD1 gene is complicated by the genomic structure of the 5'-duplicated region encoding 75% of the gene. To date, more than 90 mutations of the PKD1 gene have been reported in the European and American populations, and relatively little information is available concerning the pattern of mutations present in the Asian populations. We looked for mutations of the PKD1 gene in 51 unrelated Korean ADPKD patients, using polymerase chain reaction (PCR) with primer pairs located in the 3' single-copy region of the PKD1 gene and by single-strand conformation polymorphism (SSCP) analysis. We found three novel mutations, a G to A substitution at nucleotide 11012 (G3601S), a C to A substitution at nucleotide 11312 (Q3701X), and a C to T substitution at nucleotide 12971 (P4254S), and a single polymorphism involving a G to C substitution at nucleotide 11470 (L3753L). These mutations were not found in control individuals, and no other mutations in the 3' single-copy region of the PKD1 gene of patients with these mutations were observed. In particular, P4254S segregated with the disease phenotype. The clinical data of affected individuals from this study, and of previously reported Korean PKD1 mutations, showed that patients with frameshift or nonsense mutations were more prone to develop end-stage renal failure than those with missense mutations. Our findings indicate that many different PKD1 mutations are likely to be responsible for ADPKD in the Korean population, as in the Western population.

Detection of Hantaan and Seoul viruses by reverse transcriptase-polymerase chain reaction (RT-PCR) and restriction fragment length polymorphism (RFLP) in renal syndrome patients with hemorrhagic fever.

BACKGROUND: Hemorrhagic fever with renal syndrome (HFRS), also called Korean hemorrhagic fever (KHF), is the most common cause of acute renal failure in the Far East. Two serotypes of hantavirus, Hantaan and Seoul viruses are known pathogens for HFRS in Korea. PURPOSE: To elucidate the diagnostic applicability for the serotype diagnosis in HFRS patients, we used nested reverse transcriptase-PCR and restriction fragment length polymorphism (nRT-PCR/RFLP) to screen 2 prototype viruses, 11 virus isolates from HFRS patients, and 69 specimens obtained from 31 HFRS patients. METHODS: The nRT-PCR was performed using primers specific for the G1 segments of the Hantaan (HF3 1140-1163, HB14 1363-1342) and Seoul (SF2 809-832, SB3 1200-1177) viruses. The initial PCR products were then further amplified using nested primers for the Hantaan (HF4 1141-1164, HB13 1360-1339) and Seoul (SF7 863-884, SB1 1165-1142 ) viruses. Amplified segments were then digested with restriction enzymes specific for either Hantaan (C1a I) or Seoul (Sac I) virus sequences. RESULTS: In all cultured viruses, the serotypes identified by nRT-PCR/RFLP were consistent with those of PRNT. nRT-PCR/RFLP results indicated the presence of Hantaan virus in 10 patients and of Seoul virus in 15 patients. In 3 patients, both Hantaan- and Seoul-specific amplified bands were visualized in serially collected samples, and in 4 patients no amplicon was detected. Among 69 specimens, 55 were positive; these positive specimens were obtained between days 3 and days 33 of illness. The positive rate was not affected by the clinical phase, day of illness, or severity of HFRS. CONCLUSIONS: nRT-PCR/RFLP is a rapid and convenient method for serotype diagnosis in most HFRS patients. It could also allow detection of genetic variation of hantavirus within the same serotype.

Poor renal uptake of Tc-99m DMSA and Tc-99m MDP in a patient with Fanconi syndrome and near normal glomerular filtration rate.

The authors present a patient with Fanconi syndrome who demonstrated poor renal uptake of Tc-99m DMSA and high urinary concentration of the tracer. Tc-99m DTPA imaging was normal and the creatinine clearance was only minimally decreased. These findings suggest that Tc-99m DMSA may be accumulated in the kidney by glomerular filtration and subsequent tubular reabsorption. A Tc-99m MDP bone scan showed faint renal uptake, as well as diffuse high skeletal uptake, particularly in the spine, demonstrating that the metabolic bone disease associated with Fanconi syndrome can be one of the causes of poor renal visualization on a bone scan.

Poor renal uptake of technetium-99m-DMSA and technetium-99m-MDP in a patient with Fanconi syndrome and near normal glomerular filtration rate.

We present a patient with Fanconi syndrome who demonstrated poor renal uptake of 99mTc-DMSA and high urinary concentration of the tracer. A 99mTc-DTPA scan was normal and the creatinine clearance only minimally decreased. These findings suggest that 99mTc-DMSA may be accumulated in the kidney by glomerular filtration and subsequent tubular reabsorption, with the nonabsorbed fraction appearing in the urine. In Fanconi Syndrome the tubular reabsorption of DMSA may also be reduced, thus explaining the poor renal uptake in this patient. A 99mTc-MDP bone scan showed faint renal uptake and diffuse high uptake mainly in the spine, demonstrating that the metabolic bone disease associated with Fanconi Syndrome can be another mechanism for poor renal visualization on bone scan.