Diversity of mantids in tea plantation

Abstrac

Susceptibility baselines for the invasive mealybugs Phenacoccus manihoti and Paracoccus marginatus (Hemiptera: Pseudococcidae) in cassava ecosystem against selected neonicotinoid insecticides

In recent years, an invasive cassava mealybug Phenacoccus manihoti has been threatening cassava cultivation alongside another invasive papaya mealybug Paracoccus marginatus which invaded the country more than a decade ago. In order to evaluate their responses against the commonly used neonicotinoid insecticides: thiamethoxam 25 WG and imidacloprid 17.8 SL,  acute toxicity experiments to determine the susceptibility baselines in populations of two invasive mealybugs in the cassava agro-ecosystem, namely, cassava mealybug P. manihoti and papaya mealybug P. marginatus were performed upto 15 generations. A systemic uptake method was used for the bioassay. The LC50 values of thiamethoxam for F1 generation were 3.298 ppm whereas it was 1.066 ppm for F15 in cassava mealybug. The LC50 values of F1 generation were 2.014 ppm and that of F15 generation was 1.384 ppm when tested with imidacloprid. In the case of papaya mealybug, the LC50 values ranged from 6.138 ppm (F1) to 2.503 ppm (F15) for thiamethoxam and 7.457 ppm (F1) to 3.231 ppm (F15) for imidacloprid. All the susceptibility indices calculated were less than threefold. The rate of resistance development was negative in all cases showing that none of the tested populations harboured any resistance without insecticidal selection pressure. Tentative discriminating doses were fixed for both chemicals with the help of LC95 values obtained from the bioassay experiments, namely five ppm for both thiamethoxam and imidacloprid in the case of cassava mealybug and 10 ppm and 15 ppm, respectively, for thiamethoxam and imidacloprid in the case of papaya mealybug.          

Electro-antennographic response of Helopeltis theivora to synthetic pesticides used in tea plantations

Helopeltis theivora is considered as one of the major pest in tea plantations causing considerable economic damage. Recent control strategies against this notorious polyphagous pest mainly depend on the application of insecticides. The study is focused on the antennal response of H. theivora on exposure to different insecticides using electroantenogram (EAG). The result showed that the insects perceive quinalphos as they are frequently exposed to it. The hierarchy of the EAG response of exposed and unexposed insects was quinalphos > bifenthrin > deltamethrin > thiamethoxam

A different approach to soil analysis: Indicative studies

Soil analysis is a tool that has been employed with the primary goal of providing recommendations for soil rectification, crop productivity and for soil health management. Time tested methods like ammonium acetate extraction and diethylene triamine penta acetic acid (DTPA) are commonly used for analysis of bioavailable nutrients. However, there are some limitations to these methods as both extraction fluids are buffered to neutral or near-neutral pH. Hence extracted nutrients represent a “potential or ideal-case” fertility status of soil instead of an “actual” field status. In the ‘Regular methods’, we are overlooking the role of pH, the master variable, in determining the availability of nutrients. Hence, in ‘Modified methods’, the extraction fluid is buffered to actual soil pH. Results obtained with over 150 random samples representing a range of pH, have indicated a difference in values between regular and modified extraction methods. The modified methods (MM) of ammonium acetate and DTPA extraction adjusted to soil pH were found to be better than regular method (RM) for estimation of calcium, magnesium with ammonium acetate and iron and manganese with DTPA in alkaline soils above pH 8.0. For a complete picture of soil health, productivity and fertility, microbiological and enzymatic analysis of soils were included in the present study. Soil solution equivalent medium (SSE) was found to be the appropriate culture medium for microbial counts. A linear relationship was found between urease activity and available nitrogen of soil

The Inclination of Library Professionals to Modern Tools in the Knowledge Era

The edited volume of the book consists of ten articles covering the innovative practices of libraries in the digital environment. It includes the areas such as library network, e-resources, scholarly publishing, digital libraries, knowledge management, Web 2.0, and blockchain technology etc., that can influence the work-life of the library professionals and the academic community

Nicotine-induced survival signaling in lung cancer cells is dependent on their p53 status while its down-regulation by curcumin is independent

<p>Abstract</p> <p>Background</p> <p>Lung cancer is the most lethal cancer and almost 90% of lung cancer is due to cigarette smoking. Even though nicotine, one of the major ingredients of cigarette smoke and the causative agent for addiction, is not a carcinogen by itself, several investigators have shown that nicotine can induce cell proliferation and angiogenesis. We observed that the proliferative index of nicotine is different in the lung cancer cell lines H1299 (p53-/-) and A549 (p53+/+) which indicates that the mode of up-regulation of survival signals by nicotine might be different in cells with and without p53.</p> <p>Results</p> <p>While low concentrations of nicotine induced activation of NF-κB, Akt, Bcl2, MAPKs, AP1 and IAPs in H1299, it failed to induce NF-κB in A549, and compared to H1299, almost 100 times higher concentration of nicotine was required to induce all other survival signals in A549. Transfection of WT-p53 and DN-p53 in H1299 and A549 respectively, reversed the mode of activation of survival signals. Curcumin down-regulated all the survival signals induced by nicotine in both the cells, irrespective of their p53 status. The hypothesis was confirmed when lower concentrations of nicotine induced NF-κB in two more lung cancer cells, Hop-92 and NCI-H522 with mutant p53 status. Silencing of p53 in A549 using siRNA made the cells susceptible to nicotine-induced NF-κB nuclear translocation as in A549 DN-p53 cells.</p> <p>Conclusions</p> <p>The present study reveals a detrimental role of nicotine especially in lung cancer patients with impaired p53 status and identifies curcumin as a potential chemopreventive.</p

Associations of FTO and MC4R Variants with Obesity Traits in Indians and the Role of Rural/Urban Environment as a Possible Effect Modifier

Few studies have investigated the association between genetic variation and obesity traits in Indian populations or the role of environmental factors as modifiers of these relationships. In the context of rapid urbanisation, resulting in significant lifestyle changes, understanding the aetiology of obesity is important. We investigated associations of FTO and MC4R variants with obesity traits in 3390 sibling pairs from four Indian cities, most of whom were discordant for current dwelling (rural or urban). The FTO variant rs9939609 predicted increased weight (0.09 Z-scores, 95% CI: 0.03, 0.15) and BMI (0.08 Z-scores, 95% CI: 0.02, 0.14). The MC4R variant rs17782313 was weakly associated with weight and hip circumference (P < .05). There was some indication that the association between FTO and weight was stronger in urban than that in rural dwellers (P for interaction = .03), but no evidence for effect modification by diet or physical activity. Further studies are needed to investigate ways in which urban environment may modify genetic risk of obesity

The effect of cigarette smoke exposure on the development of inflammation in lungs, gut and joints of TNFΔARE mice

The inflammatory cytokine TNF-alpha is a central mediator in many immune-mediated diseases, such as Crohn's disease (CD), spondyloarthritis (SpA) and chronic obstructive pulmonary disease (COPD). Epidemiologic studies have shown that cigarette smoking (CS) is a prominent common risk factor in these TNF-dependent diseases. We exposed TNF Delta ARE mice; in which a systemic TNF-alpha overexpression leads to the development of inflammation; to 2 or 4 weeks of air or CS. We investigated the effect of deregulated TNF expression on CS-induced pulmonary inflammation and the effect of CS exposure on the initiation and progression of gut and joint inflammation. Upon 2 weeks of CS exposure, inflammation in lungs of TNF Delta ARE mice was significantly aggravated. However, upon 4 weeks of CS-exposure, this aggravation was no longer observed. TNF Delta ARE mice have no increases in CD4+ and CD8+ T cells and a diminished neutrophil response in the lungs after 4 weeks of CS exposure. In the gut and joints of TNF Delta ARE mice, 2 or 4 weeks of CS exposure did not modulate the development of inflammation. In conclusion, CS exposure does not modulate gut and joint inflammation in TNF Delta ARE mice. The lung responses towards CS in TNF Delta ARE mice however depend on the duration of CS exposure