Conflict Resolution Styles of XI Grade students in Delhi: An Experimental Study

The purpose of this study was to investigate the influence of interventions conducted to bring a positive change in conflict resolution styles among students of Class XI. Conflict resolution style was measured by Thomas- Kilmann Mode Instrument. Forty five students of Standard XI participated in the study. A pre-test and post-test experimental design was used. A pre-test was carried out in the beginning of the interventions to determine the conflict resolution style used by participants in their inter-personal conflicts. The interventions, in the form of group activities like removing the blocks in communication, effective usage of non-verbal communication, importance of listening, group discussion on anger management, and inculcation of constructive social skills were conducted. A post-test was carried out to measure the effects of interventions on participants’ conflict resolution styles. Results indicated that the conflict resolution style of the group was modified and transformed into a mature and constructive way of dealing with conflicts. Keywords: Conflict, Conflict Resolution, Conflict Resolution Styles, Communication. DOI: 10.7176/JEP/10-4-0

What determines the abundance of butterflies? - A short search

Butterflies neither seem to be identical nor abundant throughout the year. Their numbers decline over a period of time owing to harsh climatic changes or anthropological activities. Their appearance in the same place fluctuates with seasonal changes. With a view to this, abundance of some selected butterflies near the  University campus  in relation to the environmental factors like light, variations in temperature, humidity and rainfall was evaluated. Of the four species selected, Eurema hecabe and Catopsilia pomona (Lepidoptera: Pieridae) exhibited abundance throughout the study period while Ixias marianne (Lepidoptera: Pieridae) and Danaus chrysippus (Lepidoptera: Nymphalidae) were less abundant. Abundance was maximum during the post monsoon  months, August and September. There was a positive correlation for I. marianne with minimum temperature, relative humidity and rainfall (p<0.05) while a negative correlation was observed with mean maximum temperature (p<0.05) at both places. This was also true for C. pomona from BG for mean relative humidity at evening (p<0.05). However, there is not much variation in the abundance pattern from both the places.&nbsp

The interplay of the Notch signaling in hepatic stellate cells and macrophages determines the fate of liver fibrogenesis

Hepatic stellate cells (HSCs) known as “master producers” and macrophages as “master regulators”, are the key cell types that strongly contribute to the progression of liver fibrosis. Since Notch signaling regulates multiple cellular processes, we aimed to study the role of Notch signaling in HSCs differentiation and macrophages polarization and to evaluate its implication in liver fibrogenesis. Notch pathway components were found to be significantly upregulated in TGFβ-activated HSCs, inflammatory M1 macrophages, and in mouse and human fibrotic livers. Interestingly, inhibition of Notch using a selective γ-secretase inhibitor, Avagacestat, significantly inhibited TGFβ-induced HSC activation and contractility, and suppressed M1 macrophages. Additionally, Avagacestat inhibited M1 driven-fibroblasts activation and fibroblasts-driven M1 polarization (nitric oxide release) in fibroblasts and macrophages co-culture, and conditioned medium studies. In vivo, post-disease treatment with Avagacestat significantly attenuated fibrogenesis in CCl4-induced liver fibrosis mouse model. These effects were attributed to the reduction in HSCs activation, and inhibition of inflammatory M1 macrophages and upregulation of suppressive M2 macrophages. These findings suggest that Notch signaling plays a crucial role in HSC activation and M1/M2 polarization of macrophages in liver fibrosis. These results provide new insights for the development of novel therapies against liver fibrosis through modulation of Notch signaling

Prediction of mitochondrial proteins of malaria parasite using split amino acid composition and PSSM profile

The rate of human death due to malaria is increasing day-by-day. Thus the malaria causing parasite Plasmodium falciparum (PF) remains the cause of concern. With the wealth of data now available, it is imperative to understand protein localization in order to gain deeper insight into their functional roles. In this manuscript, an attempt has been made to develop prediction method for the localization of mitochondrial proteins. In this study, we describe a method for predicting mitochondrial proteins of malaria parasite using machine-learning technique. All models were trained and tested on 175 proteins (40 mitochondrial and 135 non-mitochondrial proteins) and evaluated using five-fold cross validation. We developed a Support Vector Machine (SVM) model for predicting mitochondrial proteins of P. falciparum, using amino acids and dipeptides composition and achieved maximum MCC 0.38 and 0.51, respectively. In this study, split amino acid composition (SAAC) is used where composition of N-termini, C-termini, and rest of protein is computed separately. The performance of SVM model improved significantly from MCC 0.38 to 0.73 when SAAC instead of simple amino acid composition was used as input. In addition, SVM model has been developed using composition of PSSM profile with MCC 0.75 and accuracy 91.38%. We achieved maximum MCC 0.81 with accuracy 92% using a hybrid model, which combines PSSM profile and SAAC. When evaluated on an independent dataset our method performs better than existing methods. A web server PFMpred has been developed for predicting mitochondrial proteins of malaria parasites (http://www.imtech.res.in/raghava/pfmpred/)

Ambient pressure upregulates nitric oxide synthase in a phosphorylated-extracellular regulated kinase– and protein kinase C–dependent manner

PurposeUsing endothelial cell/smooth muscle cell (SMC) cocultures, we have demonstrated that pressurized endothelial cell coculture inhibits SMC proliferation and promotes apoptosis, and that this effect is transferable through pressurized endothelial medium. We now hypothesized that endothelial nitric oxide synthase (eNOS) plays a significant role in mediating these pressure-induced effects.MethodsConditioned media from endothelial cells and SMCs exposed to ambient and increased pressure were transferred to recipient SMCs. We counted cells after 5 days of incubation with these media and evaluated eNOS and inducible NOS (iNOS) levels by Western blot.ResultsConditioned media from pressurized endothelial cells significantly decreased recipient SMC counts. This effect was sustained when N-nitro-L-arginine-methyl ester (L-NAME) was added to recipient cells but abolished when L-NAME was added to donor cells. SMCs were then exposed to control and pressurized conditions in monoculture or in coculture with endothelial cells. Pressure and coculture caused similar increase in iNOS levels but had no additive effect in combination. Finally, endothelial cells were exposed to control and pressurized environments. Pressure caused a 24% ± 1.6% increase in eNOS protein (P = .04, n = 12). This effect was sustained when cells were treated with L-NAME (32% ± 1.6% increase, P = .02) but abolished when endothelial cells were treated with calphostin C or PD98059 to block protein kinase C (PKC) or extracellular regulated kinase (ERK). Pressure also increased endothelial phosphorylated ERK (p-ERK) by 1.8-fold to 2.6-fold compared with control conditions after exposure of 2, 4, and 6 hours (P = .02, n = 4). This increase was sustained after pretreatment with calphostin C.ConclusionPressure modulates endothelial cell effects on SMC growth by increasing eNOS in an ERK-dependent and PKC-dependent manner.Clinical RelevanceIntimal hyperplasia is the main cause for restenosis that complicates 10% to 30% of all such vascular procedures and 30% to 40% of endovascular procedures. This article provides some novel information about smooth muscle cell/endothelial cell interaction, one of the main regulators of vascular remodeling and intimal hyperplasia. The role of endothelial cell/smooth muscle cell interaction cannot be studied well in vivo because these interactions cannot be distinguished from other factors that coexist in vivo, such as flow dynamics, matrix proteins, inflammatory factors, and interactions with other cells in the vascular wall and in the bloodstream. In this work, we use pressure as a triggering stimulus to alter in vitro endothelial behavior and identify important changes in endothelial regulation of smooth muscle cell biology. The pathways involved in this process and discussed in this article could ultimately be used to manipulate endothelial cell/smooth muscle cell interaction in clinical disease

Interplay of fission modes in mass distribution of light actinide nuclei 225,227Pa

Fission-fragment mass distributions were measured for 225,227Pa nuclei formed in fusion reactions of 19F + 206, 208Pb around fusion barrier energies. Mass-angle correlations do not indicate any quasi-fission like events in this bombarding energy range. Mass distributions were fitted by Gaussian distribution and mass variance extracted. At below-barrier energies, the mass variance was found to increase with decrease in energy for both nuclei. Results from present work were compared with existing data for induced fission of 224, 226Th and 228U around barrier energies. Enhancement in mass variance of 225, 227Pa nuclei at below-barrier energies shows evidence for presence of asymmetric fission events mixed with symmetric fission events. This is in agreement with the results of mass distributions of nearby nuclei 224, 226Th and 228U where two-mode fission process was observed. Two-mode feature of fission arises due to the shell effects changing the landscape of the potential energy surfaces at low excitation energies. The excitation-energy dependence of the mass variance gives strong evidence for survival of microscopic shell effects in fission of light actinide nuclei 225, 227Pa with initial excitation energy ~30 - 50 MeV

Detection of Molecular Markers of Antimalarial Drug Resistance in Plasmodium Falciparum from South-Western Nigeria

The widespread of drug resistant Plasmodium falciparum has led to a rise in malaria- associated mortality most especially in sub-Saharan Africa. Falciparum malaria was confirmed by microscopic examination of Giemsa-stained blood samples of patients who presented with fever in selected State Hospitals in Ogun State, Southwestern Nigeria. Molecular methods were employed to detect the markers of resistance of P. falciparum to Chloroquine, sulphadoxine/pyrimethamine,and artesunate in Ogun State, Southwestern Nigeria. DNA was extracted from patient blood using the QiaAmp DNA Blood Minikit extraction method. Nested Polymerase Chain Reaction followed by Restriction Fragment Length Polymorphisms (PCR/RFLP) were used for the detection of P. falciparum chloroquine resistance transporter (Pfcrt), P. falciparum multidrug resistance 1 (pfmdr1), P. falciparum dihydrofolate reductase (Pfdhfr), P. falciparum dihydropteroate synthase (Pfdhps) and P. falciparum sarco/endoplasmic reticulum calcium-dependent ATPase (SERCA) PfATPase6 genes. Pfcrt (K76T ) Pfmdr1 (mdr 1 ) Pfdhfr (S108N), and Pfdhps (K540E) resistant genes were detected among the isolates while resistant SERCAPfATPase6 gene which codes for artemisinin resistance was not detected in the population

Identification of allosteric hotspots regulating the ribosomal RNA binding by antibiotic resistance-conferring Erm methyltransferases

Antibiotic resistance via epigenetic methylation of ribosomal RNA is one of the most prevalent strategies adopted by multidrug resistant pathogens. The erythromycin-resistance methyltransferase (Erm) methylates rRNA at the conserved A2058 position and imparts resistance to macrolides such as erythromycin. However, the precise mechanism adopted by Erm methyltransferases for locating the target base within a complicated rRNA scaffold remains unclear. Here, we show that a conserved RNA architecture, including specific bulge sites, present more than 15 Å from the reaction center, is key to methylation at the pathogenic site. Using a set of RNA sequences site-specifically labeled by fluorescent nucleotide surrogates, we show that base flipping is a prerequisite for effective methylation and that distal bases assist in the recognition and flipping at the reaction center. The Erm–RNA complex model revealed that intrinsically flipped-out bases in the RNA serve as a putative anchor point for the Erm. Molecular dynamic simulation studies demonstrated the RNA undergoes a substantial change in conformation to facilitate an effective protein–rRNA handshake. This study highlights the importance of unique architectural features exploited by RNA to impart fidelity to RNA methyltransferases via enabling allosteric crosstalk. Moreover, the distal trigger sites identified here serve as attractive hotspots for the development of combination drug therapy aimed at reversing resistance

Hyperglycemia Induces Oxidative Stress and Impairs Axonal Transport Rates in Mice

studies to determine the effect of hyperglycemia on the neurons in the central nervous system (CNS). While olfactory dysfunction is indicated in diabetes, the effect of hyperglycemia on olfactory receptor neurons (ORNs) remains unknown. In this study, we utilized manganese enhanced MRI (MEMRI) to assess the impact of hyperglycemia on axonal transport rates in ORNs. We hypothesize that (i) hyperglycemia induces oxidative stress and is associated with reduced axonal transport rates in the ORNs and (ii) hyperglycemia-induced oxidative stress activates the p38 MAPK pathway in association with phosphorylation of tau protein leading to the axonal transport deficits.-weighted MEMRI imaging was used to determine axonal transport rates post-streptozotocin injection in wildtype (WT) and superoxide dismutase 2 (SOD2) overexpressing C57Bl/6 mice. SOD2 overexpression reduces mitochondrial superoxide load. Dihydroethidium staining was used to quantify the reactive oxygen species (ROS), specifically, superoxide (SO). Protein and gene expression levels were determined using western blotting and Q-PCR analysis, respectively.STZ-treated WT mice exhibited significantly reduced axonal transport rates and significantly higher levels of ROS, phosphorylated p38 MAPK and tau protein as compared to the WT vehicle treated controls and STZ-treated SOD2 mice. The gene expression levels of p38 MAPK and tau remained unchanged.Increased oxidative stress in STZ-treated WT hyperglycemic mice activates the p38 MAPK pathway in association with phosphorylation of tau and attenuates axonal transport rates in the olfactory system. In STZ-treated SOD-overexpressing hyperglycemic mice in which superoxide levels are reduced, these deficits are reversed