Collective Flavor Oscillations Of Supernova Neutrinos and r-Process Nucleosynthesis

Neutrino-neutrino interactions inside core-collapse supernovae may give rise to collective flavor oscillations resulting in swap between flavors. These oscillations depend on the initial energy spectra, and relative fluxes or relative luminosities of the neutrinos. It has been observed that departure from energy equipartition among different flavors can give rise to one or more sharp spectral swap over energy, termed as splits. We study the occurrence of splits in the neutrino and antineutrino spectra, varying the initial relative fluxes for different models of initial energy spectrum, in both normal and inverted hierarchy. These initial relative flux variations give rise to several possible split patterns whereas variation over different models of energy spectra give similar results. We explore the effect of these spectral splits on the electron fraction, $Y_e$, that governs r-process nucleosynthesis inside supernovae. Since spectral splits modify the electron neutrino and antineutrino spectra in the region where r-process is postulated to happen, and since the pattern of spectral splits depends on the initial conditions of the spectra and the neutrino mass hierarchy, we show that the condition $Y_e < 0.5$ required for successful r-process nucleosynthesis will lead to constraints on the initial spectral conditions, for a given neutrino mass hierarchy.Comment: 25 pages, 10 figures, added figure and improved discussion, result unchanged. Version matches to published version of JCA

Neutrinos from Stellar Collapse: Effects of flavour mixing

We study the effect of non-vanishing masses and mixings among neutrino flavours on the detection of neutrinos from stellar collapse by a water Cerenkov detector. We consider a realistic framework in which there are three neutrino flavours whose mass squared differences and mixings are constrained by the present understanding of solar and atmospheric neutrinos. We also include the effects of high dense matter within the supernova core. We find that the number of events due to the dominant process involving electron-antineutrinos may change dramatically for some allowed mixing parameters. Furthermore, contributions from charged-current scattering off oxygen atoms in the detector can be considerably enhanced due to flavour mixing; such events have a distinct experimental signature since they are backward-peaked. Hence, mixing has a non-trivial effect on the signature of neutrinos (and antineutrinos) from stellar collapse.Comment: 22 pages Latex file, with 6 postscript figures, minor changes made in tex

MSW mediated neutrino decay and the solar neutrino problem

We investigate the solar neutrino problem assuming simultaneous presence of MSW transitions in the sun and neutrino decay on the way from sun to earth. We do a global $\chi^2$-analysis of the data on total rates in Cl, Ga and Superkamiokande (SK) experiments and the SK day-night spectrum data and determine the changes in the allowed region in the \dm - \tan^2\theta plane in presence of decay. We also discuss the implications for unstable neutrinos in the SNO experiment.Comment: Final version to appear in Phys. Rev.

Testing the solar LMA region with KamLAND data

We investigate the potential of 3 kiloTon-years(kTy) of KamLAND data to further constrain the $\Delta m^2$ and $\tan^2\theta$ values compared to those presently allowed by existing KamLAND and global solar data. We study the extent, dependence and characteristics of this sensitivity in and around the two parts of the LMA region that are currently allowed. Our analysis with 3 kTy simulated spectra shows that KamLAND spectrum data by itself can constrain $\Delta m^2$ with high precision. Combining the spectrum with global solar data further tightens the constraints on allowed values of $\tan^2\theta$ and $\Delta m^2$. We also study the effects of future neutral current data with a total error of 7% from the Sudbury Neutrino Observatory. We find that these future measurements offer the potential of considerable precision in determining the oscillation parameters (specially the mass parameter).Comment: 16 pages, to appear in J Phys.

Triphala inhibits both in vitro and in vivo xenograft growth of pancreatic tumor cells by inducing apoptosis

<p>Abstract</p> <p>Background</p> <p>Triphala is commonly used in Ayurvedic medicine to treat variety of diseases; however its mechanism of action remains unexplored. This study elucidates the molecular mechanism of Triphala against human pancreatic cancer in the cellular and in vivo model.</p> <p>Methods</p> <p>Growth-inhibitory effects of Triphala were evaluated in Capan-2, BxPC-3 and HPDE-6 cells by Sulphoradamine-B assay. Apoptosis was determined by cell death assay and western blotting. Triphala was administered orally to nude mice implanted with Capan-2 xenograft. Tumors were analyzed by immunohistochemistry and western blotting.</p> <p>Results</p> <p>Exposure of Capan-2 cells to the aqueous extract of Triphala for 24 h resulted in the significant decrease in the survival of cells in a dose-dependent manner with an IC50 of about 50 μg/ml. Triphala-mediated reduced cell survival correlated with induction of apoptosis, which was associated with reactive oxygen species (ROS) generation. Triphala-induced apoptosis was linked with phosphorylation of p53 at Ser-15 and ERK at Thr-202/Tyr-204 in Capan-2 cells. Above mentioned effects were significantly blocked when the cells were pretreated with an antioxidant N-acetylcysteine (NAC), suggesting the involvement of ROS generation. Pretreatment of cells with pifithrin-α or U0126, specific inhibitors of p53 or MEK-1/2, significantly attenuated Triphala-induced apoptosis. Moreover, NAC or U0126 pretreatment significantly attenuated Triphala-induced p53 transcriptional activity. Similarly, Triphala induced apoptosis in another pancreatic cancer cell line BxPC-3 by activating ERK. On the other hand, Triphala failed to induce apoptosis or activate ERK or p53 in normal human pancreatic ductal epithelial (HPDE-6) cells. Further, oral administration of 50 mg/kg or 100 mg/kg Triphala in PBS, 5 days/week significantly suppressed the growth of Capan-2 pancreatic tumor-xenograft. Reduced tumor-growth in Triphala fed mice was due to increased apoptosis in the tumors cells, which was associated with increased activation of p53 and ERK.</p> <p>Conclusion</p> <p>Our preclinical studies demonstrate that Triphala is effective in inhibiting the growth of human pancreatic cancer cells in both cellular and in vivo model. Our data also suggests that the growth inhibitory effects of Triphala is mediated by the activation of ERK and p53 and shows potential for the treatment and/or prevention of human pancreatic cancer.</p

Performance of the ocean state forecast system at Indian National Centre for Ocean Information Services

The reliability of the operational Ocean State Forecast system at the Indian National Centre for Ocean Information Services (INCOIS) during tropical cyclones that affect the coastline of India is described in this article. The performance of this system during cyclone Thane that severely affected the southeast coast of India during the last week of December 2011 is reported here. Spec-tral wave model is used for forecasting the wave fields generated by the tropical cyclone and vali-dation of the same is done using real-time automated observation systems. The validation results indicate that the forecasted wave parameters agree well with the measurements. The feedback from the user community indicates that the forecast was reliable and highly useful. Alerts based on this operational ocean state forecast system are thus useful for protecting the property and lives of the coastal communities along the coastline of India. INCOIS is extending this service for the benefit of the other countries along the Indian Ocean rim

A Novel Triterpenoid Isolated from the Root Bark of Ailanthus excelsa Roxb (Tree of Heaven), AECHL-1 as a Potential Anti-Cancer Agent

We report here the isolation and characterization of a new compound Ailanthus excelsa chloroform extract-1 (AECHL-1) (C(29)H(36)O(10); molecular weight 543.8) from the root bark of Ailanthus excelsa Roxb. The compound possesses anti-cancer activity against a variety of cancer cell lines of different origin.AECHL-1 treatment for 12 to 48 hr inhibited cell proliferation and induced death in B16F10, MDA-MB-231, MCF-7, and PC3 cells with minimum growth inhibition in normal HEK 293. The antitumor effect of AECHL-1 was comparable with that of the conventional antitumor drugs paclitaxel and cisplatin. AECHL-1-induced growth inhibition was associated with S/G(2)-M arrests in MDA-MB-231, MCF-7, and PC3 cells and a G(1) arrest in B16F10 cells. We observed microtubule disruption in MCF-7 cells treated with AECHL-1 in vitro. Compared with control, subcutaneous injection of AECHL-1 to the sites of tumor of mouse melanoma B16F10 implanted in C57BL/6 mice and human breast cancer MCF-7 cells in athymic nude mice resulted in significant decrease in tumor volume. In B16F10 tumors, AECHL-1 at 50 microg/mouse/day dose for 15 days resulted in increased expression of tumor suppressor proteins P53/p21, reduction in the expression of the oncogene c-Myc, and downregulation of cyclin D1 and cdk4. Additionally, AECHL-1 treatment resulted in the phosphorylation of p53 at serine 15 in B16F10 tumors, which seems to exhibit p53-dependent growth inhibitory responses.The present data demonstrate the activity of a triterpenoid AECHL-1 which possess a broad spectrum of activity against cancer cells. We propose here that AECHL-1 is a futuristic anti-cancer drug whose therapeutic potential needs to be widely explored for chemotherapy against cancer

Predicting disease risk areas through co-production of spatial models: the example of Kyasanur Forest Disease in India’s forest landscapes

Zoonotic diseases affect resource-poor tropical communities disproportionately, and are linked to human use and modification of ecosystems. Disentangling the socio-ecological mechanisms by which ecosystem change precipitates impacts of pathogens is critical for predicting disease risk and designing effective intervention strategies. Despite the global “One Health” initiative, predictive models for tropical zoonotic diseases often focus on narrow ranges of risk factors and are rarely scaled to intervention programs and ecosystem use. This study uses a participatory, co-production approach to address this disconnect between science, policy and implementation, by developing more informative disease models for a fatal tick-borne viral haemorrhagic disease, Kyasanur Forest Disease (KFD), that is spreading across degraded forest ecosystems in India. We integrated knowledge across disciplines to identify key risk factors and needs with actors and beneficiaries across the relevant policy sectors, to understand disease patterns and develop decision support tools. Human case locations (2014–2018) and spatial machine learning quantified the relative role of risk factors, including forest cover and loss, host densities and public health access, in driving landscape-scale disease patterns in a long-affected district (Shivamogga, Karnataka State). Models combining forest metrics, livestock densities and elevation accurately predicted spatial patterns in human KFD cases (2014–2018). Consistent with suggestions that KFD is an “ecotonal” disease, landscapes at higher risk for human KFD contained diverse forest-plantation mosaics with high coverage of moist evergreen forest and plantation, high indigenous cattle density, and low coverage of dry deciduous forest. Models predicted new hotspots of outbreaks in 2019, indicating their value for spatial targeting of intervention. Co-production was vital for: gathering outbreak data that reflected locations of exposure in the landscape; better understanding contextual socio-ecological risk factors; and tailoring the spatial grain and outputs to the scale of forest use, and public health interventions. We argue this inter-disciplinary approach to risk prediction is applicable across zoonotic diseases in tropical settings

Identification of TBX15 as an adipose master trans regulator of abdominal obesity genes

Background: Obesity predisposes individuals to multiple cardiometabolic disorders, including type 2 diabetes (T2D). As body mass index (BMI) cannot reliably differentiate fat from lean mass, the metabolically detrimental abdominal obesity has been estimated using waist-hip ratio (WHR). Waist-hip ratio adjusted for body mass index (WHRadjBMI) in turn is a well-established sex-specific marker for abdominal fat and adiposity, and a predictor of adverse metabolic outcomes, such as T2D. However, the underlying genes and regulatory mechanisms orchestrating the sex differences in obesity and body fat distribution in humans are not well understood. Methods: We searched for genetic master regulators of WHRadjBMI by employing integrative genomics approaches on human subcutaneous adipose RNA sequencing (RNA-seq) data (n similar to 1400) and WHRadjBMI GWAS data (n similar to 700,000) from the WHRadjBMI GWAS cohorts and the UK Biobank (UKB), using co-expression network, transcriptome-wide association study (TWAS), and polygenic risk score (PRS) approaches. Finally, we functionally verified our genomic results using gene knockdown experiments in a human primary cell type that is critical for adipose tissue function. Results: Here, we identified an adipose gene co-expression network that contains 35 obesity GWAS genes and explains a significant amount of polygenic risk for abdominal obesity and T2D in the UKB (n = 392,551) in a sex-dependent way. We showed that this network is preserved in the adipose tissue data from the Finnish Kuopio Obesity Study and Mexican Obesity Study. The network is controlled by a novel adipose master transcription factor (TF), TBX15, a WHRadjBMI GWAS gene that regulates the network in trans. Knockdown of TBX15 in human primary preadipocytes resulted in changes in expression of 130 network genes, including the key adipose TFs, PPARG and KLF15, which were significantly impacted (FDR < 0.05), thus functionally verifying the trans regulatory effect of TBX15 on the WHRadjBMI co-expression network. Conclusions: Our study discovers a novel key function for the TBX15 TF in trans regulating an adipose co-expression network of 347 adipose, mitochondrial, and metabolically important genes, including PPARG, KLF15, PPARA, ADIPOQ, and 35 obesity GWAS genes. Thus, based on our converging genomic, transcriptional, and functional evidence, we interpret the role of TBX15 to be a main transcriptional regulator in the adipose tissue and discover its importance in human abdominal obesity.Peer reviewe