HI content in galaxies in loose groups

Gas deficiency in cluster spirals is well known and ram-pressure stripping is considered the main gas removal mechanism. In some compact groups too gas deficiency is reported. However, gas deficiency in loose groups is not yet well established. Lower dispersion of the member velocities and the lower density of the intra-group medium in small loose groups favour tidal stripping as the main gas removal process in them. Recent releases of data from HI Parkes all sky survey (HIPASS) and catalogues of nearby loose groups with associated diffuse X-ray emission have allowed us to test this notion. In this paper, we address the following questions: (a) do galaxies in groups with diffuse X-ray emission statistically have lower gas content compared to the ones in groups without diffuse X-ray emission? (b) does HI deficiency vary with the X-ray luminosity of the loose group in a systematic way? We find that (a) galaxies in groups with diffuse X-ray emission, on average, are HI deficient, and have lost more gas compared to those in groups without X-ray emission; the later are found not to have significant HI deficiency; (b) no systematic dependence of the HI deficiency with X-ray luminosity is found. Ram pressure assisted tidal stripping and evaporation by thermal conduction are the two possible mechanisms to account for this excess gas loss.Comment: 9 pages, 4 figures, accepted in MNRA

A molecular line survey of W3(OH) and W3 IRS 5 from 84.7 to 115.6 GHz: Observational data and analyses

We have carried out observations toward the W3 complex and G34.3+0.15 using the TRAO14 m radio telescope to examine in detail the chemical variations occurring while molecular clouds evolve from the prestellar to the H II region phase. Observations include spectral surveys of these objects between 84.7 and 115.6 GHz; mapping observations toward W3(OH) with the emissions of CS (2-1), HCN (1-0), HNC (1-0), and HCO+ (1-0); and mapping of CS (2-1) emission toward W3 IRS 5. Chemical model calculations are used to estimate the age of W3(OH) by comparing with the fractional abundances of detected molecules. We found that G34.3+0.15 and W3(OH) are at a similar evolutionary stage, although large differences in the fractional abundances are found in CH3CN and HC3N. Overall, the properties of the detected species and abundances in three regions support the view that chemistry varies as molecular clouds evolve from a cold, collapsing phase to a high-temperature phase, such as the hot core and H II phase. Chemical model calculations for W3(OH) indicate that the evolutionary age of the cloud is 10(4)-10(5) yr with temperature in the range 10-60 K

MOLECULAR PREVALENCE OF PORCINE CIRCOVIRUS 2 INFECTION: FOREMOST REPORT IN SOUTHERN STATES OF INDIA

Porcine circovirus 2 (PCV2) is the emerging viral pathogen in the swine associated with multi-systemic clinical and subclinical outcomes. This study aimed to detect the molecular and serological prevalence of PCV2 infection in the southern states of India. A total of 434 random samples comprising serum (n=273), pooled postmortem tissues (n=109) and rectal, vaginal, and nasal swabs (n=52) and were collected from PCV2 suspected and healthy swine populations of Tamil Nadu, Kerala, Andhra Pradesh, Telangana, and Puducherry states in India from 2019 to 2021 were screened for PCV2 by specific polymerase chain reaction (PCR) assay. Of 434 samples screened, 12.2% (n=53) showed positivity to PCV2 genome. Statistical analysis of the molecular prevalence of PCV2 within breed, age, sex, and vaccination status revealed no significant (p>0.05) difference but there was a significant (p<0.05) difference in the prevalence of PCV2 among healthy and suspected swine populations. Suspected pigs had a significantly higher prevalence of PCV2 in comparison to healthy. ELISA-based PCV2 antibody screening in 176 non-vaccinated serum samples revealed a seropositivity of 44.8% (n=79). The molecular and seroprevalence of PCV2 is alarming in southern states of India, which necessitates the need for genotypic characterization and phylogenetic analysis and development of candidate vaccine for implementation of suitable prevention and control measures

Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells

Genomic instability is a common feature of cancer etiology. This provides an avenue for therapeutic intervention, since cancer cells are more susceptible than normal cells to DNA damaging agents. However, there is growing evidence that the epigenetic mechanisms that impact DNA methylation and histone status also contribute to genomic instability. The DNA damage response, for example, is modulated by the acetylation status of histone and non-histone proteins, and by the opposing activities of histone acetyltransferase and histone deacetylase (HDAC) enzymes. Many HDACs overexpressed in cancer cells have been implicated in protecting such cells from genotoxic insults. Thus, HDAC inhibitors, in addition to unsilencing tumor suppressor genes, also can silence DNA repair pathways, inactivate non-histone proteins that are required for DNA stability, and induce reactive oxygen species and DNA double-strand breaks. This review summarizes how dietary phytochemicals that affect the epigenome also can trigger DNA damage and repair mechanisms. Where such data is available, examples are cited from studies in vitro and in vivo of polyphenols, organosulfur/organoselenium compounds, indoles, sesquiterpene lactones, and miscellaneous agents such as anacardic acid. Finally, by virtue of their genetic and epigenetic mechanisms, cancer chemopreventive agents are being redefined as chemo- or radio-sensitizers. A sustained DNA damage response coupled with insufficient repair may be a pivotal mechanism for apoptosis induction in cancer cells exposed to dietary phytochemicals. Future research, including appropriate clinical investigation, should clarify these emerging concepts in the context of both genetic and epigenetic mechanisms dysregulated in cancer, and the pros and cons of specific dietary intervention strategies

A Systematic Study of Coding Performance in a MIMO–STBC–OFDM Link

Restricted Access.MIMO–STBC–OFDM systems mitigate inter symbol interference and frequency-selective fading caused by multi-path propagation in modern high-data-rate wireless communication. Error correction codes use redundancy to correct errors that still occur. No systematic analysis of their performance using a common link configuration is found in the literature. We fill this gap in this simulation study using a common MIMO–STBC–OFDM communication link, transferring data at a symbol rate of 100 Mbps. We find that (a) for all code rates, low-density parity-check code performs best with BPSK and to an extent with QPSK and (b) ½-rate convolutional code works well for all symbol mapping schemes