Comparison of INSAT-3D retrieved total column ozone with ground-based and AIRS observations over India.

Ozone plays an important role in the thermal structure and chemical composition of the atmosphere. The present study compares the temporal and spatial distributions of Total Column Ozone (TCO) over the Indian sub-continent retrieved from a geostationary Indian National Satellite (INSAT-3D) and Atmospheric Infrared Sounder (AIRS). The INSAT-3D TCO values are also evaluated against the Dobson spectrophotometer observations at two locations. The inter-comparison results reveal a good correlation of 0.8, the bias of -5 DU, and Root Mean Square Error (RMSE) of 15 DU approximately between the TCO retrieved from INSAT-3D and AIRS. The lowest RMSE and highest correlation coefficient were found in the pre-monsoon season. The INSAT-3D and AIRS show reasonable agreement with the RMSE varying between 10 and 30 DU. On the other hand, evaluation of the INSAT-3D TCO with the ground-based observations from Dobson spectrophotometers located at New Delhi and Varanasi showed fair agreement with a maximum monthly mean correlation coefficient of 0.68 and 0.76, respectively, and RMSE varying from 11 to 16 DU for both the stations. The seasonal distribution of TCO and its variation over the Indian region has also been studied using INSAT-3D and AIRS data. The analysis exhibits strong seasonal variations, with higher values in pre-monsoon season and minimum values in winter season. The noticeable seasonal variability of TCO can be attributed to complex combination of photochemical and dynamical processes in the troposphere and stratosphere. The main objectives of the study are to compare the INSAT-3D TCO with two independent ground-based Dobson spectrophotometer observations and Atmospheric Infrared Sounder (AIRS) aboard NASA's Aqua satellite.

The effects of atorvastatin in experimental autoimmune uveitis.

AIM: To investigate the effect of atorvastatin (Lipitor), a commonly used drug for dyslipidaemia in experimental autoimmune uveitis (EAU). METHODS: 48 B10-RIII mice were immunised with human interphotoreceptor retinoid binding protein (IRBP) peptide p161-180. They were divided into three groups of 16 each and treated orally once daily for 14 days; group one received phosphate buffered saline (control group), group two received 1 mg/kg of atorvastatin (low dose group), and group three received 10 mg/kg (high dose). On day 14 lymph nodes, spleens, and right eyes were harvested. RNA was extracted from lymph nodes for RNase protection assay (RPA) to determine proinflammatory (IL-1 alpha and IL-1 beta), Th1 (TNF-alpha, IL-2, IL-12), and Th2 (IL-4, IL-5, and IL-10) cytokine levels. Protein was extracted from spleens for western blot to detect the expression of phosphorylated signal transducer and activator of transcription (STAT) 4 and STAT6. The severity of inflammation in enucleated eyes was graded by a masked observer. Paired t test was performed for the mean difference in histological scoring between treated groups and the immunised control group. RESULTS: Surprisingly, atorvastatin did not modulate the immune response. The proinflammatory cytokines, IL-1 alpha and IL-1 beta, and Th1 cytokines, TNF-alpha and IL-2, were upregulated equally in control and atorvastatin treated groups. IL-12 and Th2 cytokines were not upregulated in all three groups. Western blot analysis showed high levels of phosphorylated STAT4, but not STAT6 protein in the control and atorvastatin treated groups. Mean differences in histological scoring between treated groups and the immunised control group were not statistically significant. CONCLUSIONS: Atorvastatin treatment had no effect on Th1 and Th2 cytokine transcription. Although histological grading suggested mildly decreased inflammation in the high dose treated group, the equivalence of cytokine expression in all groups suggests that the statins may not modulate IRBP induced uveoretinitis.

Complete nucleotide sequence of an Indian strain of Japanese encephalitis virus: sequence comparison with other strains and phylogenetic analysis.

The RNA genome of an Indian strain of Japanese encephalitis virus (JEV), GP78, was reverse transcribed and the cDNA fragments were cloned in bacterial plasmids. Nucleotide sequencing of the cDNA clones covering the entire genome of the virus established that the GP78 genome was 10,976 nucleotides long. An open reading frame of 10,296 bases, capable of coding for a 3,432 amino acid polyprotein, was flanked by 95- and 585-base long 5'- and 3'-non-coding regions, respectively. When compared with the nucleotide sequence of the JaOArS982 strain, the JEV GP78 genome had a number of nucleotide substitutions that were scattered throughout the genome except for the 5'-noncoding region, the sequence of which was fully conserved. Comparison of the complete genome sequences of different JEV isolates showed a 1.3-4.1% nucleotide sequence divergence among them, which resulted in 0.6-1.8% amino acid sequence divergence. Analysis based on the complete genome sequences of different JEV isolates showed that the GP78 isolate from India was phylogenetically closer to the Chinese SA14 isolate.

d-limonene chemoprevention of hepatocarcinogenesis in AKR mice: inhibition of c-jun and c-myc.

We have studied the chemopreventive effect of d-limonene, a monoterpene monocyclic compound, against N-nitrosodiethylamine (NDEA) alone and along with phenobarbital (PB) induced hepatocarcinogenesis in AKR mice. Histopathological analysis clearly indicates the maintenance of normal features when the mice were given limonene 15 days prior to carcinogen treatment. The immunohistochemical analysis of c-jun and c-myc oncoprotein shows an increased protein expression (2-3 fold) in NDEA and NDEA-PB mediated hepatocarcinogenesis after 60 days of NDEA treatment. Our earlier work by northern blot analysis has already indicated an increased transcription of c-jun and c-myc in NDEA mediated hepatocarcinogenesis. However, such overexpression of c-myc and c-jun both at mRNA and oncoprotein levels has been completely inhibited when d-limonene was used along with NDEA or NDEA-PB. Thus, the present investigation explains the anti-tumour effect of d-limonene for the first time on the level of oncogene expression in NDEA and NDEA-PB mediated hepatocarcinogenesis.

Induction of lung carcinogenesis in AKR-mice by N-nitrosodiethylamine/phenobarbitone, associated with high expression of c-myc and c-jun oncoproteins.

Lung carcinogenesis was induced in AKR mice using N-nitrosodiethylamine (NDEA). Tumors were detected in 46.8% of mice provided with 100 ppm NDEA in drinking water. The incidence of tumors was increased to 64.2% when the same carcinogenesis was promoted by phenobarbitone (PB). Lung tumor bearing mice showed no tumors in other organs. Characteristic features of these lung tumors are: (i) appearance of tumors within a short period of time i.e. less than 75 days; (ii) no increase in the number and size of tumors with the increase in dose and duration of treatment of carcinogen; (iii) the same histological type was maintained in more than 80% of tumors. Animals that received treatment for 75-125 days showed no significant advancement in the stage of carcinogenesis in comparison to the 50-75 days treatment period. Moreover, mice which received treatment for 125-150 days, did not have any neoplastic lesions in lungs, but they consisted of liver tumors generally. Expression of oncoproteins, c-myc and c-jun, was detected in all lung tumors but the expression of c-myc protein was more than that of c-jun and both of these oncoproteins were enhanced by the promoter, PB. Highest level of expression of c-myc and c-jun was detected within the period of 50-75 days, whereafter it was decreased significantly within the period of 75-125 days and 125-150 days of treatment. Thus, the results indicate that c-myc/c-jun might be involved in the development of lung cancer in AKR mice, but may not have any role in the maintenance of the malignant phenotype of lungs.

Differential expression of c-jun and c-myc in N-nitroso diethylamine-induced hepatic oncogenesis in AKR mice.

Expression of c-jun, c-myc, c-fos and c-Ha-ras was examined and correlated with the various stages of N-nitrosodiethylamine (NDEA)-induced hepatocarcinogenesis in male AKR mice. The treated groups were given NDEA 100 ppm, in drinking water for 120 days. The histopathology along with the expression of oncogenes were studied at different durations of treatment such as after 1 day, 3 days, 6 days, 9 days, 15 days, 20 days 30 days, 60 days, 90 days and 120 days of treatment. The results of histological investigation indicate mild hyperplasia and anisonucleosis at 30 days of treatment and prominent pathological features from 60 days onwards until the appearance of hepatocarcinoma at 120 days even without the development of any preneoplastic or neoplastic nodule. The results of the Northern blot hybridization clearly indicate an increased expression of c-jun from 15 days onwards. This overexpression of c-jun at such an early stage indicates its association with the events earlier than the neoplastic changes. However, the persistent overexpression of c-jun at all durations of treatment indicates its association with the events during the later stage of hepatocarcinogenesis, whereas c-myc overexpression starts from 30 days of treatment and persists until the end of the experiment, i.e. 120 days of treatment. However, the results of densitometric quantification indicate that the extent of increase expression of c-myc is less than that of c-jun expression until 1 month of treatment, after which the induction of c-myc exceeds the expression of c-jun. Thus, the overexpression of c-myc from 2 months onwards might be playing a critical role in maintenance of the malignant phenotype. On the other hand, the expressions of c-fos and c-Ha-ras do not have any alteration during NDEA treatment. Thus, our data demonstrate the involvement of c-jun and c-myc in NDEA-induced hepatocarcinogenesis in AKR mice.