Far Infrared Study of IRAS 00494+5617 & IRAS 05327-0457

High angular resolution far-infrared observations at 143 & 185 \micron, using the TIFR 1-m balloon borne telescope, are presented for two Galactic star forming complexes associated with IRAS 00494+5617 and 05327-0457. The latter map also reveals the cold dust in OMC-3. The HIRES processed IRAS maps at 12, 25, 60 & 100 micron have also been presented for comparison. Both these regions are illuminated at the edges by high mass stars with substantial UV flux.The present study is aimed at quantifying the role of the nearby stars vis-a-vis embedded young stellar objects in the overall heating of these sources. Based on the FIR observations at 143 & 185 micron carried out simultaneously with almost identical angular resolution, reliable dust temperature and optical depth maps have been generated for the brighter regions of these sources. Radiative transfer modeling in spherical geometry has been carried out to extract physical parameters of these sources by considering the observational constraints like : spectral energy distribution, angular size at different wavelengths, dust temperature distribution etc. It has been concluded that for both IRAS 00494+5617 and IRAS 05327-0457, the embedded energy sources play the major role in heating them with finite contribution from the nearby stars. The best fit model for IRAS 00494+5617 is consistent with a simple two phase clump-interclump picture with $\sim$ 5% volume filling factor (of clumps) and a density contrast of $\approx$ 80

Hepatitis C virus infection is the major cause of severe liver disease in India

The present study describes the status of hepatitis C virus infection in 167 patients with severe forms of liver diseases in India. The anti-HCV positivity rate was recorded as 43%, 47% and 42% in patients with FHF, SAHF and CAH respectively. HBV and HCV coinfection was recorded in 28% of FHF, 43% of SAHF and 75% of the CAH cases. Superinfection of HCV in HBsAg carriers was recorded in 54% cases of FHF, 60% of SAHF and 42% of the CAH. None of these 167 patients was positive of HAV-IgM. Further, 27.7% of FHF, 26.4% of SAHF and 15.2% of CAH cases were neither HBV nor HCV markers positive. These can be labelled as non-A, non-B and nonC infections

Hepatitis B virus replication in patients with chronic liver diseases

One hundred and seventy five subjects with chronic liver diseases which included patients with chronic active hepatitis (90), liver cirrhosis (31) and asymptomatic hepatitis B carriers (54), were included in the study. Hepatitis B virus (HBV) specific DNA-polymerase activity and HBe-markers were tested as markers of HBV-multiplicaiton. In HBsAg positive samples, DNA-P activity was positive in 44.4% of the HBV carriers, 52.9% of the patients with chronic active hepatitis and 81.8% of the patients with liver cirrhosis. The corresponding figures for the presence of HBeAg in these groups were 18.5, 26.5 and 45.5% respectively. Virus multiplication was also observed in 41.1 and 44.4% patients with chronic active hepatitis and liver cirrhosis respectively, in the absence of HBsAg. The results of the present study show that hepatitis B virus is the most important etiological factor of chronic liver diseases in India. Most of our patients of chronic liver diseases seems to have contacted HBV infection as young adults and the mode of transmission is likely to be horizontal rather than vertical. The virus replicating markers correlate well with the severity of the liver injury and decreased with the age. DNA-P activity is a more sensitive marker of viral multiplication than HBeAg. Viral multiplication was also found to occur in the absence of the usual HBV markers. Continued viral multiplication in patients with chronic active hepatitis and liver cirrhosis is implicated in continued liver injury and progressive liver disease

Significance of anti-pre-S antibodies in patients with fulminant hepatic failure

Anti-pre-S antibody was tested in 38 sera from patients with fulminant hepatitis (positive for HBsAg and/or IgM anti-HBc) using a specific solid phase enzyme linked immunosorbent assay (ELISA). Anti-pre-S activity was detected in 50 percent sera samples positive for HBsAg but negative for IgM antiHBc. There were 12.5% sera positive for both HBsAg as well as IgM anti-HBc and 75% sera negative for HBsAg but positive for IgM anti-HBc. The prevalence of HBV-specific DNA-polymerase activity was high in all the three groups whereas anti-HBs positivity was low. Anti-pre-S activity was observed both in the presence as well as in the absence of DNA-polymerase activity. High-anti-pre-S level in fulminant hepatitis B patients was assumed to be implicated in the fast clearance of HBsAg from circulation

Far Infrared Observations of the Galactic Star Forming Regions associated with IRAS 00338+6312 and RAFGL 5111

Two Galactic star forming regions, one in a very early phase of evolution and another evolved one, associated with the IRAS sources 00338+6312 and 03595+5110 (RAFGL 5111) respectively have been studied in detail. These sources have been mapped simultaneously in two far infrared bands at 143 & 185 \micron), with about 1.5 arcmin angular resolution, using the TIFR 100 cm balloon borne telescope. The HIRES processed IRAS maps at 12, 25, 60 & 100 \micron, have been used for comparison. Whereas IRAS 00338+6312 is resolved only in the TIFR bands, RAFGL 5111 is very well resolved in both the TIFR bands, as well as in at least 3 IRAS bands. The neighbouring fainter source IRAS 04004+5114 has also been resolved in the TIFR bands. Taking advantage of the identical beams in the two TIFR bands at 143 & 185 \micron, dust colour temperature, $T(143/185)$, and optical depth, $\tau_{150}$, maps have been generated for RAFGL 5111. These maps show interesting structural details. Radiative transfer modelling in spherical geometry has been carried out for individual sources. The best fit models are in good agreement with the observed spectral energy distribution (SED), radio continuum data etc. Another scheme of radiative transfer through the interstellar dust-gas cloud including the heavier elements has been used to predict ionic nebular line emission, which are in reasonable agreement with the measurements for RAFGL 5111. An important conclusion from the present study is that, for all the three sources (IRAS 00338+6312; 03595+5110; and 04004+5114, a faint source in the neighbourhood of RAFGL 5111), the best fit to the observed SED is obtained for a uniform density ($n(r) \sim r^0$) cloud

A customized monocyte cDNA microarray for diagnosis of rheumatoid arthritis and prognosis of anti-TNF-α therapy

Background In rheumatoid arthritis (RA) macrophages (Mf) play a pivotal role. They become highly activated in synovitis and at the cartilage–pannus junction. Furthermore, therapeutic neutralization of molecules produced by activated Mf lead to clinical improvement in RA, and circulating monocytes (MO) of the peripheral blood in patients with RA spontaneously express proinflammatory genes (IL-1β, IL-6, TNF). Methods A custom RA-MO cDNA microarray was generated using differentially expressed genes obtained from gene subtraction and from comparative whole genome wide U133A analysis in normal donors, active and anti-TNF-α created RA patients. Genes were selected using MAS 5.0, multtest and PAM. The custom microarray consists of 313 genes including guide dots, and positive (housekeeping genes and spike controls) and negative controls for image and statistical analysis. Each probe was spotted in 16 replicates. Results The RA-MO chipset-II was validated using the following: non-stimulated and LPS, PMA, Vit.D3+LPS, PMA+LPS stimulated U937 cells; nonstimulated and LPS stimulated healthy donor MO; MO from normal donors (n = 3) and RA patients before and during anti-TNF-α treatment (n = 5 each); and synovial tissue from normal individuals (n = 2) and RA patients (n = 2). Not only LPS/PMA regulated genes but also RA specific and anti-TNF-α regulated genes were validated. In addition, we could clarify whether these genes are differentially transcribed only in MO or whether they can also be found in RA tissue Mf. Our data indicate a high degree of reproducibility that is sufficient for diagnostic applications and therapy monitoring. Conclusion The RA-MO chipset-II microarray is competitive and flexible for enlargement of the number of genes. The current gene selection will contribute to validating the role of monocytes in disease activity, to therapeutic interventions, and may improve the knowledge on the regulation of pathways in activated monocytes in chronic inflammation

GASP XVIII: Star formation quenching due to AGN feedback in the central region of a jellyfish galaxy

We report evidence for star formation quenching in the central 8.6 kpc region of the jellyfish galaxy JO201 which hosts an active galactic nucleus, while undergoing strong ram pressure stripping. The ultraviolet imaging data of the galaxy disk reveal a region with reduced flux around the center of the galaxy and a horse shoe shaped region with enhanced flux in the outer disk. The characterization of the ionization regions based on emission line diagnostic diagrams shows that the region of reduced flux seen in the ultraviolet is within the AGN-dominated area. The CO J$_{2-1}$ map of the galaxy disk reveals a cavity in the central region. The image of the galaxy disk at redder wavelengths (9050-9250 \overset{\lower.5em\circ}{\mathrm{A}}) reveals the presence of a stellar bar. The star formation rate map of the galaxy disk shows that the star formation suppression in the cavity occurred in the last few 10$^8$ yr. We present several lines of evidence supporting the scenario that suppression of star formation in the central region of the disk is most likely due to the feedback from the AGN. The observations reported here make JO201 a unique case of AGN feedback and environmental effects suppressing star formation in a spiral galaxy.Comment: Author's accepted manuscrip

Fulminant hepatitis in a tropical population: clinical course, cause, and early predictors of outcome

The profiles of patients with fulminant hepatic failure (FHF) from developing countries have not been reported earlier. The current study was conducted prospectively, at a single tertiary care center in India, to document the demographic and clinical characteristics, natural course, and causative profile of patients with FHF as well as to define simple prognostic markers in these patients. Four hundred twenty-three consecutive patients with FHF admitted from January 1987 to June 1993 were included in the study. Each patient's serum was tested for various hepatotropic viruses. Univariate Cox's regression for 28 variables, multivariate Cox's proportional hazard regression, stepwise logistic regression, and Kaplan-Meier survival analysis were done to identify independent predictors of outcome at admission. All patients presented with encephalopathy within 4 weeks of onset of symptoms. Hepatotropic viruses were the likely cause in most of these patients. Hepatitis A (HAV), hepatitis B (HBV), hepatitis D (HDV) viruses, and antitubercular drugs could be implicated as the cause of FHF in 1.7% (n = 7), 28% (n = 117), 3.8% (n = 16), and 4.5% (n = 19) patients, respectively. In the remaining 62% (n = 264) of patients the serological evidence of HAV, HBV, or HDV infection was lacking, and none of them had ingested hepatotoxins. FHF was presumed to be caused by non-A, non-B virus(es) infection. Sera of 50 patients from the latter group were tested for hepatitis E virus (HEV) RNA and HCV RNA. In 31 (62%), HEV could be implicated as the causative agent, and isolated HCV RNA could be detected in 7 (19%). Two hundred eighty eight (66%) patients died. Approximately 75% of those who died did so within 72 hours of hospitalisation. One quarter of the female patients with FHF were pregnant. Mortality among pregnant females, nonpregnant females, and male patients with FHF was similar (P > .1). Univariate analysis showed that age, size of the liver assessed by percussion, grade of coma, presence of clinical features of cerebral edema, presence of infection, serum bilirubin, and prothrombin time prolongation over controls at admission were related to survival (P < .01). The rapidity of onset of encephalopathy and cause of FHF did not influence the outcome. Cox's proportional hazard regression showed age ≥ 40 years, presence of cerebral edema, serum bilirubin ≥ 15 mg/dL, and prothrombin time prolongation of 25 seconds or more over controls were independent predictors of outcome. Ninety-three percent of the patients with three or more of the above prognostic markers died. The sensitivity, specificity, positive predictive value, and the negative predictive value of the presence of three or more of these prognostic factors for mortality was 93%, 80%, 86%, and 89.5%, respectively, with a diagnostic accuracy of 87.3%. We conclude that most of our patients with FHF might have been caused by hepatotropic viral infection, and non-A, non-B virus(es) seems to be the dominant hepatotropic viral infection among these patients. They presented with encephalopathy within 4 weeks of the onset of symptoms. Pregnancy, cause, and rapidity of onset of encephalopathy did not influence survival. The prognostic model developed in the current study is simple and can be performed at admission