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An experiment was conducted at National Seed Project, University of Agricultural Sciences, GKVK, Bangalore during rabi 2017-18 to evaluate the influence planting geometry and mother plant nutrition on seed yield and quality of parental lines (Male: CML-451 and female : CAL-1443) of maize hybrid MAH 14-5. The maize parental lines were sown in the field with four fertilizer doses viz., F1-112.5:70:50 NPKha-1 + 10 kg ZnSo4, F2-150:70:50 NPK ha-1+ 10 kg ZnSo4, F3-187:70:50 NPK ha-1+ 10 kg ZnSo4, F4-225:70:50 NPK ha-1+ 10 kg ZnSo4 and at four different spacing viz., S1- 30×20 cm, S2- 45×20 cm, S3- 60×20 cm, S4-60×30 cm. Among the interactions, the highest field emergence in male observed in S2F3 (98.7%), plant population S1F4 (97.3), plant height S3F2 (138.3 cm) at the time of harvest, number of seeds per cob S3F2 (138.2), cob weight S3F2(138.8 cm), seed weight per cob in S3F2 (475.2 gm), seed yield per hectare in S2F3 (29.45 q/hac), whereas in case of female highest field emergence was observed in S3F1 (97.3%), plant population S1F2 (104.3 cm), plant height S3F2 (164.5 cm) at the time of harvest, number of seeds per cob S3F2 (275.3), cob weight (138.8 cm), seed weight per cob in S3F2 (273.2 gm), seed yield per hectare in S2F3 (25.96 q/hac). In male, the lowest field emergence in male observed in S3F3 (95.7%), plant population S4F4 (38.0), plant height S3F2 (114.0 cm) at the time of harvest, number of seeds per cob S3F2 (138.2), cob weight (138.8 cm), seed weight per cob in S4F1 (275.2 gm), seed yield per hectare in S2F3 (19.06 q/hac), whereas in case of female lowest field emergence was observed in S3F1 (94.3%), plant population S1F2 (38.7 cm), plant height S3F4 (136.2 cm) at the time of harvest, number of seeds per cob S3F1 (217.3), cob weight S4F1(207.9 cm), seed weight per cob in S4F1 (142.2 gm), seed yield per hectare in S4F1 (11.58q/hac).

An experiment was conducted to assess the physiological performance of groundnut (Arachis hypogaea L.) in storage during 2016-2017 to evaluate the influence of storage containers and desiccants on longevity of groundnut Cv. G2-52. The groundnut is stored both in the form of pods and kernels, and they were stored in four different packaging materials like PICS (Perdue improved crop storage) bag, HDPE (High density polythene bag) bag, polythene bag (700 gauge), and gunny bag. Among the interactions T1 (pod stored in PICS bag) showed maximum seed quality parameters like germination (81.17%), seedling dry weight (294.7 mg), dehydrogenase activity (0.440 OD value) with lowest electrical conductivity (dS/m). Whereas the lowest germination (55.17), seedling dry weight (131 mg), dehydrogenase activity (0.142 OD value), with highest electrical conductivity (1.410 dS/m) were recorded in T14 (kernel stored in gunny bag) at the eight month of storage period.

A sound mind in a healthy body – this phrase articulates the interconnectedness of the psyche and physic. It is necessary to observe that every student has peculiar strengths and different needs. Thus it remains resourceful to acknowledge the campus environments that serve as perpetual entities of adaptation to students mentally and physically.

Previously, Bithionol (BT) was shown to enhance the chemosensitivity of ovarian cancer cell lines to cisplatin treatment. In the present study, we focused on the anti-tumor potential of the BT-paclitaxel combination when added to a panel of ovarian cancer cell lines. This in vitro study aimed to 1) determine the optimum schedule for combination of BT and paclitaxel and 2) assess the nature and mechanism(s) underlying BT-paclitaxel interactions. The cytotoxic effects of both drugs either alone or in combination were assessed by presto-blue cell viability assay using six human ovarian cancer cell lines. Inhibitory concentrations to achieve 50% cell death (IC50) were determined for BT and paclitaxel in each cell line. Changes in levels of cleaved PARP, XIAP, bcl-2, bcl-xL, p21 and p27 were determined via immunoblot. Luminescent and colorimetric assays were used to determine caspases 3/7 and autotaxin (ATX) activity. Cellular reactive oxygen species (ROS) were measured by flow cytometry. Our results show that the efficacy of the BT-paclitaxel combination depends upon the concentrations and sequence of addition of paclitaxel and BT. Pretreatment with BT followed by paclitaxel resulted in antagonistic interactions whereas synergistic interactions were observed when both drugs were added simultaneously or when cells were pretreated with paclitaxel followed by BT. Synergistic interactions between BT and paclitaxel were attributed to increased ROS generation and enhanced apoptosis. Decreased expression of pro-survival factors (XIAP, bcl-2, bcl-xL) and increased expression of pro-apoptotic factors (caspases 3/7, PARP cleavage) was observed. Additionally, increased expression of key cell cycle regulators p21 and p27 was observed. These results show that BT and paclitaxel interacted synergistically at most drug ratios which, however, was highly dependent on the sequence of the addition of drugs. Our results suggest that BT-paclitaxel combination therapy may be effective in sensitizing ovarian cancer cells to paclitaxel treatment, thus mitigating some of the toxic effects associated with high doses of paclitaxel.

In terms of the concept of 'drug repurposing', we focused on pharmaceutical-grade Bithionol (BT) as a therapeutic agent against ovarian cancer. Our recent in-vitro study provides preclinical data suggesting a potential therapeutic role for BT against recurrent ovarian cancer. BT was shown to cause cell death by caspases-mediated apoptosis. The present preliminary study further explores the antitumor potential of pharmaceutical-grade BT in an in-vivo xenograft model of human ovarian cancer. Nude Foxn1 mice bearing SKOV-3 human ovarian tumor xenografts were treated with titrated doses of BT and the therapeutic efficacy of pharmaceutical BT was determined using bioluminescence imaging. BT-induced changes in cell proliferation and apoptosis were evaluated by Ki-67 immunochemical staining and TUNEL assay. The effect of BT on autotaxin levels in serum, ascitic fluid, and tumor tissue was assessed by colorimetric and western blot techniques. BT treatment did not show antitumor potential or enhanced survival time at any of the doses tested. No apparent signs of toxicity were observed with any of the doses tested. Immunohistological analysis of tumor sections did not indicate a significant decrease in cellular proliferation (Ki-67 assay). An increase in apoptosis (by TUNEL assay) was observed in all BT-treated mice compared with vehicle-treated mice. Although BT did not show significant antitumor activity in the present study, the ability of BT to induce apoptosis still makes it a promising therapeutic agent. Further confirmatory and optimization studies are essential to enhance the therapeutic effects of BT.

This study is based on the buyer‟s behaviour towards gingelly oil. A psychometric response scale primarily used in questionnaires to obtain participant‟s preferences or degree of agreement with a statement or set of statements. Likert scales are a non‐comparative scaling technique and are unidimensional (only measure a single trait) in nature. Respondents are asked to indicate their level of agreement with a given statement by way of an ordinal scale.The influence of personal characteristics and buyer‟s preference factors on the behaviour as well as the relationship between buyer and purchasing behaviour of gingelly oil are examined. This study shows that, overall, the consumers have positive attitude towards using of gingelly oil on their daily food.

INTRODUCTION: Cancer progression and tumorigenesis have been linked to alterations in cellular metabolic pathways of lipid and cholesterol synthesis in many cancers. Increased levels of cholesterol esters (CE) have been reported in breast cancer, leukemia, glioma and prostate cancer, but not exploited in detail in ovarian and endometrial cancers. Inside cells, excess free cholesterol is esterified by acyl-CoA cholesterol acyltransferase (ACAT) and stored as cholesteryl ester (CE) in lipid droplets (LDs). Cholesteryl ester accumulation may be a consequence of loss of tumor suppressor PTEN and subsequent activation of PI3K/AKT pathway as observed in pancreatic cancer. In the present study, we focused on the role of ACAT and cholesterol esters in altered cholesterol metabolism in ovarian/endometrial cancer cell lines. METHODS: We studied the effect of abrogation of cholesterol esterification either by an ACAT-1 inhibitor/shRNA knockdown or via inhibition of PI3K/AKT/mTOR pathways and subsequent effect on ovarian/endometrial cancer cells proliferation, invasion, cell migration and tumorigenesis. The expression of ACAT was studied at the protein and mRNA levels in a panel of ovarian/ endometrial cancer cell lines and also in normal and ovarian cancer clinical samples. ACAT expression was assessed by western blotting, ELISA, quantitative RT-PCR and immunostaining techniques. RESULTS: Our results reveal an elevated expression of ACAT-1 at both protein and mRNA levels in ovarian and endometrial cancer cell lines as compared to primary cells. Our results also provide preliminary data on involvement of ACAT and cholesterol esters in the progression and metastasis of ovarian cancer. CONCLUSION: These studies may aid in the development of new biomarkers or treatment targets for ovarian/endometrial cancer. Citation Format: Vijayalakshmi N. Ayyagari, Xinjia Wang, Laurent Brard. Studies on role of acyl-CoA cholesterol acyltransferase (ACAT) expression in ovarian/endometrial cancer progression - An invitro study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4416. doi:10.1158/1538-7445.AM2017-4416

Background Drug resistance is a cause of ovarian cancer recurrence and low overall survival rates. There is a need for more effective treatment approaches because the development of new drug is expensive and time consuming. Alternatively, the concept of ‘drug repurposing’ is promising. We focused on Bithionol (BT), a clinically approved anti-parasitic drug as an anti-ovarian cancer drug. BT has previously been shown to inhibit solid tumor growth in several preclinical cancer models. A better understanding of the anti-tumor effects and mechanism(s) of action of BT in ovarian cancer cells is essential for further exploring its therapeutic potential against ovarian cancer. Methods The cytotoxic effects of BT against a panel of ovarian cancer cell lines were determined by Presto Blue cell viability assay. Markers of apoptosis such as caspases 3/7, cPARP induction, nuclear condensation and mitochondrial transmembrane depolarization were assessed using microscopic, FACS and immunoblotting methods. Mechanism(s) of action of BT such as cell cycle arrest, reactive oxygen species (ROS) generation, autotaxin (ATX) inhibition and effects on MAPK and NF-kB signalling were determined by FACS analysis, immunoblotting and colorimetric methods. Results BT caused dose dependent cytotoxicity against all ovarian cancer cell lines tested with IC50 values ranging from 19 μM – 60 μM. Cisplatin-resistant variants of A2780 and IGROV-1 have shown almost similar IC50 values compared to their sensitive counterparts. Apoptotic cell death was shown by expression of caspases 3/7, cPARP, loss of mitochondrial potential, nuclear condensation, and up-regulation of p38 and reduced expression of pAkt, pNF-κB, pIκBα, XIAP, bcl-2 and bcl-xl. BT treatment resulted in cell cycle arrest at G1/M phase and increased ROS generation. Treatment with ascorbic acid resulted in partial restoration of cell viability. In addition, dose and time dependent inhibition of ATX was observed. Conclusions BT exhibits cytotoxic effects on various ovarian cancer cell lines regardless of their sensitivities to cisplatin. Cell death appears to be via caspases mediated apoptosis. The mechanisms of action appear to be partly via cell cycle arrest, ROS generation and inhibition of ATX. The present study provides preclinical data suggesting a potential therapeutic role for BT against recurrent ovarian cancer.

Diseases due to non-toxigenic strains of Corynebacterium diphtheriae are being increasingly reported. These diseases have been found to occur in vaccinated individuals. We report two cases of diphtheria with myocarditis and polyneuritis caused by non-toxigenic strains of C. diphtheriae. The virulence factors of this organism and the pitfalls in diagnosis have also been discussed.

Introduction: ‘Drug Repurposing’ promises to be a successful concept for the treatment of many diseases. We focused on Bithionol (BT), a clinically approved antiparasitic drug for use as a therapeutic agent against ovarian cancer. BT has been shown to inhibit solid tumor growth in several preclinical cancer models by targeting autotaxin (ATX). Methods: In the present study, we determined the anti-tumor effect of BT and its mechanism of action against a panel of ovarian cancer cell lines. First, we studied the cytotoxic effect of BT against a panel of ovarian cancer cell lines (A2780 & A2780-CDDP OVACAR-3, SKOV-3, IGROV-1, and IGROV-1CDDP). We identified the type of cell death i.e. apoptotic vs. necrosis, and examined markers of apoptosis and necrosis. Mechanism(s) of action were studied in terms of reactive oxygen species (ROS) generation, autotoxin (ATX) inhibition and MAPK signaling. In addition, we studied the sensitizing effect of BT on cisplatin cytotoxicity. Results: Our results have shown that BT causes dose dependent cytotoxicity against all the cell lines tested with IC50 values ranging from 20μM - 60μM. The order of ranking in terms of sensitivity to BT is A2780 > SKOV-3 > OVACAR-3>, IGROV-1. Cisplatin resistant variants of A2780 and IGROV-1 have shown almost similar IC50 values to their sensitive variant. Apoptotic cell death was observed at low concentration and early time points whereas necrosis was observed at high concentrations and later time points. Apoptotic cell death was shown by expression of caspases 3,7, increased homogenous caspases 3/7 activity, loss of mitochondrial potential, cPARP expression, DNA condensation, up-regulation of p38 and down regulation of XIAP. At higher concentrations, BT caused down-regulation of caspases3/7 activity and increased LDH activity indicative of necrosis. Sensitization studies with BT showed that pre-treatment of ovarian cancer cell lines with BT for 24 hrs enhanced cisplatin cytotoxicity by 20 - 80%. Interestingly, cisplatin resistant variants of A2780 and IGROV-1 were more sensitive to cisplatin upon BT pre-treatment as compared to their sensitive variants. The order of ranking in terms of enhanced sensitivity to cisplatin upon BT pre-treatment was A2780-CDDP > A2780 > OVCAR-3 > IGROV-1CDDP > IGROV-1 >SJOV-3. BT treatment resulted in increased ROS generation. Treatment with antioxidant ascorbic acid resulted in partial restoration of cell viability. In addition, dose and time dependent inhibition of ATX was observed. Conclusions: Our results demonstrate the cytotoxic effect of BT on various ovarian cancer cells and the mechanism of actions appears to be partly via ROS generation and inhibition of ATX. Pre-treatment with BT resulted in enhanced cytotoxicity to cisplatin especially in cisplatin resistant variants. In view of these results, BT can be an effective adjunct agent along with cisplatin for ovarian cancer treatment. Citation Format: Vijayalakshmi N. Ayyagari, Laurent Brard. Studies on antitumor effects of bithionol on ovarian cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2121. doi:10.1158/1538-7445.AM2013-2121

Introduction: Our previous work has shown that the loss of Rab25 occurs in estrogen receptor (ER) and progesterone receptor (PR) negative breast cancer cell lines and human tumor samples and seems to correlate with an active Ras pathway. Loss of Rab25 cooperates with mutant Ras to promote tumorigenesis. RIN1 is a protein inhibitor of Ras, and our current works confirms that Rab25 binds to RIN1 and cooperates to inhibit Ras. Rab25 also has multiple effects on microRNAs. Materials and Methods: Cell culture -RAO-1-4 cell lines was grown in DFCI-1 medium. Immunoprecipitation- Protein extracts from RAO-1, RAO-2, and RAO-3/Rab25 were tested for RIN1expression. Immunoprecipitated extracts were then assayed by western blot for RAB25 expression. Chemiluminescence Assay- Cell extract from MDA-MB-231 cells with shRIN1 was used. These cells contained no Rab25 as well. Recombinant RIN1 and recombinant Rab25 were tested in various combinations for ras inhibition using the Active Motif kit. MicroRNA assay- RNA was extracted from RAO-2, RAO-4, and RAO-4/Rab25 and sent to Phalanx Biotech for microRNA profiling. Results: 1. Rab25 binds to RIN1 in a ternary complex with Ras. 2. Rab25 coopeates with RIN1 in an additive manner to inhibit Ras. 3. Rab25 expression impacts several microRNAs including 29b, 100, 138, 146a, 205, 524-5p, 762, 1246, 1260b, 1307, 1826, 3172, 3175, and 3178. Conclusions: 1. Rab25 is a tumor modulator. It can regulate tumor growth and angiogenesis through inhibition of ras in cooperation with RIN1. 2. Our data previous indicated that Rab25 could localize to the nucleus, and it appears to effect the expression of several microRNAs. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4161. doi:1538-7445.AM2012-4161

Introduction: Our previous work has shown that the loss of Rab25 occurs in estrogen receptor (ER) and progesterone receptor (PR) negative breast cancer cell lines and human tumor samples and seems to correlate with an active ras pathway. We have examined the expression levels of rab25 in breast tissue and have investigated the mechanism by which Rab25 exerts its anti-tumorigenic effect. Loss of Rab25 cooperates with mutant Ras to promote tumorigenesis. HIF-1α levels are reduced in Rab25 expressing cells. We have assessed Rab25 binding to the HIF-1α promoter and localized Rab25 to the nucleus, suggesting a novel mechanism for Rab25's antitumor activity and a novel function for Rab25. Materials and Methods: Cell culture – Normal mammary tissue and the RAO-3 cell line was grown in DFCI-1 medium. Cells were transduced with retroviral supernatant and selected. Expression of Rab25 in transduced cells was determined by RT-PCR and western blot. qPCR analysis- Expression of HIF-1α and Rab25 were quantified using real-time PCR with fluorescence detection. Luciferase report assay – We obtained the HIF-1α promoter fragment and inserted the promoter sequence in the pGL4 luciferase vector and the Luciferase Assay was then performed. Western blot- Protein extracts from both cytosolic and nuclear fraction were tested for Rab25 expression. Immunofluorescence- Frozen mammary tissue slides were stained with luminal and basal markers as well as antibody for Rab25 to confirm localization of Rab25 in both luminal and basal mammary epithelium. Results: 1. High level expression of Rab25 was found in luminal epithelium in normal human breast tissue. Basal epithelium also expressed Rab25. 2. Tumorigenic mammary epithelial cell lines, RAO-3 and RAO-4, have lost Rab 25 expression with nearly 1/10,000 the level of Rab25 of normal mammary basal epithelium. 3. Rab25 localizes to the nucleus and reduces luciferase activity from the HIF-1α promoter. 4. Expression of Rab25 substantially reduces HIF-1α levels. Conclusions: 1. Rab25 is a complex molecule that has been described as an intracellular transport protein. 2. It is also a tumor modulator. It can regulate tumor growth and angiogenesis. 3. Rab25 expression can be detected in both luminal epithelium and basal epithelium. 4. Our data indicate novel functions for Rab25 including reduction in HIF-1α expression and localization to the nucleus. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2111. doi:10.1158/1538-7445.AM2011-2111

Introduction: Our previous work has shown that the loss of Rab25 occurs in estrogen receptor (ER) and progesterone receptor (PR) negative breast cancer cell lines and human tumor samples and seems to correlate with an active ras pathway. We have expressed Rab25 in several hormonally insensitive breast cancer cell lines and have demonstrated marked reduction in tumor growth. Histologically, the tumor cells appear smaller, and angiogenesis is significantly reduced. We have investigated the mechanism by which Rab25 exerts its anti-tumorigenic effect. Loss of Rab25 cooperates with mutant Ras to promote tumorigenesis in primary human mammary epithelial cells (HMEC). HIF1-alpha levels are markedly increased with loss of Rab25 if Ras is overexpressed. Rab25 is expressed in both luminal and basal mammary epithelium at similar levels. The loss of rab25 enhances VEGF-A secretion and VEGFR1 expression. Monoclonal antibodies can be potentially used to target these pathways which appear to be active in Rab25 negative tumors. Materials and Methods: Cell culture - MDA-MB-231 cells were grown in DME medium with 10% FBS, and Rao-3 cell line and HMEC were grown in DFCI-1 medium. Cells were transduced with retroviral supernatant and selected. Expression of RAB25 in transduced cells was determined by RT-PCR and western blot. Silencing of Rab25-Rab-25 was silenced in RAO-2 cells by pENTRTM/H1/TO siRNA system (Invitrogen, Carlsbad, CA). Our shRNA sequences are designed using the BLOCK-iTTM RNAi Designer. The most effective silencer of Rab25 was selected on the basis of testing 3 sequence pairs. The double-stranded oligos were inserted into the pENTR/H1/TO vector and transfected into cells. Silencing of Rab25 in transduced cells was confirmed by RT-PCR and Western blot. qPCR analysis- Expression of HIF1-alpha was quantified using real-time PCR with fluorescence detection. Western blot- Western blot was performed on cell extracts for rab25 and ras. Immunohistochemistry - CK5/6 served as a basal maker, and CK18 served as a luminal maker for co-staining with Rab25 in human mammary gland. In vivo tumor formation assay − 5 × 106 cells in 0.1 ml PBS were injected into the left mammary fat pad of five week-old female nude mice. Mice were monitored for the following 7 weeks for tumor volume. Therapeutic assays- Cell lines were incubated with anti-VEGF-A, anti-VEGFR1, or both, and cell numbers were tabulated over 5 days. Results: 1) Rab25 loss cooperated with Ras to promote tumorigenesis in several donors. 2) HIF1α levels rose significantly with loss of Rab25 and Ras co-expression. 3) Rab25 is expressed in both basal and luminal normal mammary epithelium. 4) Both anti-VEGF-A and anti-VEGFR1 antibodies have therapeutic implications for Rab25 negative breast cancer cell lines. Conclusions: Rab25 is a tumor suppressor that antagonizes Ras and may be part of an important therapeutic pathway. Its loss may serve as therapeutic marker for certain types of breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3073.