Search

Light-induced electron-spin-resonance (LESR) spin density in a perovskite solar cell (PSC) is ascribed to photo-induced charges accumulated at the interface of the perovskite and the hole transport layer (HTL). The LESR spin density was observed to be decreased as the temperature was lowered from room temperature to 170 K in a PSC; below ∼170 K, no LESR was found. Meanwhile, the photocurrent showed only an ∼25% decrease between room temperature and 170 K. The comparison of LESR in temperature-dependence with transient or steady photocurrents suggested that the decrease in photocurrent at the low temperatures stems mainly from trapping of delocalized holes at the interface of perovskite and HTL. [ABSTRACT FROM AUTHOR]

Human lung adenocarcinoma, the most prevalent form of lung cancer, is characterized by many molecular abnormalities. K-ras mutations are associated with the initiation of lung adenocarcinomas, but K-ras-independent mechanisms may also initiate lung tumors. Here, we find that the runt-related transcription factor Runx3 is essential for normal murine lung development and is a tumor suppressor that prevents lung adenocarcinoma. Runx3−/− mice, which die soon after birth, exhibit alveolar hyperplasia. Importantly, Runx3−/− bronchioli exhibit impaired differentiation, as evidenced by the accumulation of epithelial cells containing specific markers for both alveolar (that is SP-B) and bronchiolar (that is CC10) lineages. Runx3−/− epithelial cells also express Bmi1, which supports self-renewal of stem cells. Lung adenomas spontaneously develop in aging Runx3+/− mice (∼18 months after birth) and invariably exhibit reduced levels of Runx3. As K-ras mutations are very rare in these adenomas, Runx3+/− mice provide an animal model for lung tumorigenesis that recapitulates the preneoplastic stage of human lung adenocarcinoma development, which is independent of K-Ras mutation. We conclude that Runx3 is essential for lung epithelial cell differentiation, and that downregulation of Runx3 is causally linked to the preneoplastic stage of lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

To optimize management of chronic liver disease (CLD), a simple and noninvasive test to determine oesophageal varices (EV) and liver fibrosis is necessary. We performed a cohort study in a single tertiary care centre in order to devise a simple index reflecting EV and liver fibrosis. We derived an index reflecting EV which resulted from portal hypertension (the first part) and evaluated the index’s ability to detect liver fibrosis which resulted in portal hypertension (the second part). Five hundred fifty-six patients (the first part, n = 409, mean age = 55.4 years, EV prevalence = 34.0%; the second part, n = 147, mean age = 48.8 years, cirrhosis prevalence = 12.9%) with virus-related CLD were included. P2/MS [(platelet count [109/L])2/(monocyte fraction [%] × segmented neutrophil fraction [%])] was derived to detect EV. The area under the receiver-operating characteristic curve (AUROC) of P2/MS was 0.916 (95% confidence interval, 0.879–0.954) for detecting EV, and 0.905 (0.862–0.947) for detecting high-risk EV (grade ≥ II or with red colour signs). P2/MS had AUROCs of 0.952 (0.904–0.999) and 0.873 (0.792–0.955) for histological cirrhosis (METAVIR F4) and significant fibrosis (METAVIR F2–F4), respectively, which were significantly greater than those of AST-to-platelet count ratio index (0.658, P < 0.001; 0.644, P = 0.003) and FIB-4 (0.776, P = 0.031; 0.707, P = 0.026). The predictive values of P2/MS were maintained at similar accuracy in subsequent validation sets. Our study suggests that P2/MS comprising only the complete blood count results is an efficient and noninvasive marker reflecting the presence of EV and the grade of liver fibrosis in patients with virus-related CLD. An independent external validation of P2/MS is required. [ABSTRACT FROM AUTHOR]

Endothelium-derived nitric oxide (NO) plays an important role in transducing the effects of angiogenic factors. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase (NOS). We used a murine model of hindlimb ischemia to investigate whether genetic or metabolic changes in ADMA levels could impair angiogenic response in vivo. Hindlimb ischemia was surgically induced in C57BL/6J mice, apo E-deficient mice, or transgenic mice overexpressing dimethylarginine dimethylaminohydrolase (DDAH). Some animals were also treated with the NOS antagonist L-nitro-arginine, or the NO precursor L-arginine. Angiogenesis was quantified in the hindlimb skeletal muscle by capillary/myocyte ratio. Plasma or tissue ADMA levels were measured by HPLC. In normal mice, hindlimb ischemia increased tissue ADMA twofold, and reduced DDAH and NOS expression. This was associated with a reduced NOS activity (by over 80%) three days following surgery. On day seven, a threefold increase in DDAH expression and a fall in tissue ADMA levels were associated with a sevenfold increase in NOS activity, whereas NOS expression did not increase above baseline. In DDAH transgenic mice, the elevation of ADMA and decrement in NOS activity was blunted during hindlimb ischemia. Plasma ADMA levels were increased in apo E-mice (1.79 ± 0.45 versus 1.07 ± 0.08 μmol/l; p = 0.008). Capillary index was significantly reduced in apo Emice up to seven weeks after surgery (0.25 ± 0.05 versus 0.62 ±; 0.08; p > 0.001). The effect of hypercholesterolemia on capillary index was reversed by L-arginine, and (in wild-type mice) mimicked by administration of the NOS antagonist L-nitro-arginine. In conclusion, metabolic or genetic changes in plasma and tissue ADMA levels affect tissue NO production and angiogenic response to ischemia. [ABSTRACT FROM AUTHOR]

To analyze the aberrant expression of cell cycle-related proteins and their biological significance in relation to cirrhosis, we compared the cirrhotic patterns induced by two different types of cirrhotic agents, CCl4 and thioacetamide (TAA) in rats. CCl4 or TAA treatment was given to rats for 8 or 30 weeks, respectively, and the livers were removed at 9, 20, and 30 weeks after the experiment began. The TAA-induced fibrotic pattern was different from the CCl4-induced one, in terms of the formation of fibrous connective tissue and the proliferation of bile ductule cells. Cholangiofibrosis and clear cell foci were also observed in TAA-treated rats at 30 weeks. Histological examination revealed severe cirrhotic changes at 9 weeks in CCl4-treated rats and at 30 weeks in TAA-treated rats. Immunoblotting for cyclin D1, E, A, B, and proliferating cell nuclear antigen (PCNA) and their counterpart protein kinases (CDK2, 4, and CDC2) showed significant overexpression in rats with severely cirrhotic livers. The p53 tumor suppressor protein increased dramatically in the CCl4-treated group, while it was not detected in the livers of TAA-treated rats. Upregulation of p21WAF1, a CDK inhibitory protein, was detected in TAA-treated rats, but not in CCl4-treated rats. Immunohistochemical data for cyclin D1, E, and PCNA were well correlated with immunoblotting data; these proteins were increased in hepatocytes surrounding the cirrhotic lesions, suggesting that hepatocyte regeneration is correlated with cell cycle-related protein expression in cirrhotic liver. In the TAA-treated rats, the expression of these proteins was increased both in hepatocytes and in ductule cells. Our data suggest that liver cirrhosis induced by CCl4 or TAA is associated with alterations in cell cycle-related proteins, and that the expression of these proteins is responsible for hepatocyte regeneration in the damaged liver and may be involved in liver carcinogenesis. [ABSTRACT FROM AUTHOR]

There has not been much evidence about rehabilitation results for the infants with hearing problems under age 1 even though the 1-3-6 principle of early diagnosis and intervention was accepted worldwide. In this study, we tried to reveal auditory verbal intervention effects for the infants with hearing problems followed by the principle. A total of 50 babies and their caregivers participated. The average hearing thresholds of the babies were worse than 80 dB HL(B) and they were fitted HAs or CIs except 5 babies with no hearing prosthesis. The average age of the participants at the initial assessment was 7.3 months and the average age at the final assessment was 12.6 months. After the initial assessment, their development was closely followed in the 8 developmental areas of sound responses, listening skills, receptive & expressive language, speech development, oral functions, social interactions, and cognitive communication with auditory verbal approach. Their initial developmental rate was 0.55 and the rate had been accelerated up to 1.8, however, after 6 monthintervention, final development rate was 0.76 which had not reached to the normal rate of 1. There were large individual differences as expected, in average, the area of cognitive communication was the most developed area while the area of speech was the least developed area at the end of the intervention. Auditory verbal approach was suitable for the babies as well as their caregivers and could provide valid and timely information about the effects of prostheses they were wearing and the timing of changing devices for the babies. It would be more informative with longer period of the intervention. [ABSTRACT FROM AUTHOR]