PROSPEK PERDAGANGAN KOPI ROBUSTA INDONESIA DI PASAR INTERNASIONAL

This research aims to predict the trades of Indonesian coffee in the international market for the next decade.This research used secondary data, specifically the export volume of robusta coffee from 1975 to 2011.Forecasting process was done by using the method of linear time series analysis with ARIMA models. Theresults showed that the model for maximum export volume of robusta coffee was Yt = Yt-1 + 6.646 – 0.5028(Wt-1 – Wt-2) – 0,4134 (Wt-2 – Wt-3) + et.. It was predicted in the next 10 years, from 2012 to 2021, the exportvolume of the Indonesian coffee will increase. The growth of the export volume of robusta coffee will be1.6% each year. Finally, in 2021 the export volume of robusta coffee will reach 493.295 tons

Analysis of spontaneously reported cutaneous adverse drug reactions in a tertiary care teaching hospital in South India

Background: Skin is the most common organ involved in adverse reactions due to drugs. With newer drugs released into market every year, there is changing pattern of the reported cutaneous adverse drug reactions (ADRs). In order to ensure safer use of medicines in patients, there is need for continuous monitoring of ADRs. This is a retrospective study to analyse spontaneously reported cutaneous ADRs.Methods: All the cutaneous ADRs reported between January 2017 and September 2018 were analysed for clinical patterns, suspected medications, causality, severity and preventability.Results: Of the 1035 reports received during the study period, 232 (22.41%) included cutaneous reactions. 113 (48.7%) were male and 119 (51.29%) were female. Maculopapular rash 70 (30.17%), pruritus 31 (13.36%), palmar plantar erythrodysesthesia 30 (12.93%), acne 19 (8.19%), urticaria 16 (6.89%) and fixed drug eruptions (FDE) 13 (5.6%) were the common clinical patterns. Antimicrobial agents followed by anticancer drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), hormones and related drugs, and antiepileptic drugs were the common suspected group of drugs. Causality assessment as done by WHO-UMC scale showed that 3 (1.29%) were certainly related, 174 (75%) were probably related and 55 (23.7%) were possibly related to the suspected medication.Conclusions: Cutaneous ADRs are most frequently reported ADRs in the present study. With newer drugs released into market, there is a need for continuous monitoring of use of drugs to promote safer use of medicines in patients

Ondansetron versus palonosetron: a comparative study on efficacy and safety in prevention of postoperative nausea and vomiting

Background: Postoperative nausea and vomiting (PONV) is a major complication in patients who undergo surgery under general anaesthesia. Various drug regimens and antiemetic interventions have been tried from time-to-time for prevention of PONV but with a variable success rate. This study compares the safety and efficacy of ondansetron and palonosetron in preventing PONV in such patients.Methods: A prospective study was conducted in 60 ASA grades - I and II patients of either sex, aged between 20 to 50 years, scheduled for elective surgery under general anaesthesia, 30 of who received 4 mg ondansetron and the remaining 30 received 0.05 mg palonosetron intravenously 5 minutes before induction of anaesthesia. Postoperatively they were observed for 24 hours for complete response, any episodes of nausea and vomiting, their severity, need for rescue antiemetic and side effects. After the study, results were compiled and the data was analysed using Student’s T test. P value 0.5). Complete antiemetic response was 60% in ondansetron group and 83% in palonosetron group. There was no significant statistical difference between both the groups in causing headache (p >0.5) and dizziness (p >0.05).Conclusions: Our study concludes that the antiemetic efficacy is comparable for both ondansetron and palonosetron in the given doses in preventing PONV and none is superior. Both the study drugs had almost the same adverse effect profile

Variation in transpiration efficiency and its related traits in a groundnut (Arachis hypogaea L.) mapping population

Transpiration efficiency (TE) has been recognized as an important source of yield variation under drought stress in groundnut. Here the variation for TE is evaluated in a set of 318 recombinant inbred lines (RILs) of groundnut at F8 generation, derived from a cross between a high TE (ICGV 86031) and a low TE (TAG 24) parent, and the value of specific leaf area (SLA), SPAD chlorophyll meter readings (SCMR) and carbon isotope discrimination (Δ13C) as surrogates of TE are measured. Transpiration efficiency was measured gravimetrically in the 318 RILs and parents under progressive soil drying in a pot culture in two post-rainy seasons. Large and consistent variation for TE existed among the RILs across years. The overall distribution of TE among the RILs indicated that TE was governed by dominant and additive genes. Surrogates SLA and SCMR, were measured prior, during and after completion of the drought period, whereas Δ13C was measured on the dried tissue after harvest. Transpiration efficiency was negatively associated with SLA after the completion of stress treatment (r2=0.15) and Δ13C in leaves (r2=0.13) and positively associated with SCMR during stress (r2=0.17). These associations, all fairly weak, were significant only in 2004. None of these relationships was found in 2005. Although the heritability of SCMR during 2005 was relatively higher than that of TE, and although SCMR has previously been used to identify contrasting germplasm for TE, the stress-dependence of the relationship with TE, and the poor regression coefficients (r2) with that RIL population, do not confer that these surrogates are adequately robust enough in that population. Though more time consuming, a direct gravimetric evaluation for TE appeared to be more reliable

Nuclear deformation and the two neutrino double-\beta decay in ^{124,126}Xe,^{128,130}Te, ^{130,132}Ba and ^{150}Nd isotopes

The two neutrino double beta decay of $^{124,126}$Xe,$^{128,130}$Te, $^{130,132}$Ba and $^{150}$Nd isotopes is studied in the Projected Hartree-Fock-Bogoliubov (PHFB) model. Theoretical 2$\nu$ $\beta^{-}\beta ^{-}$ half-lives of $^{128,130}$Te, and $^{150}$Nd isotopes, and 2$\nu \beta^{+}\beta^{+}$, 2$\nu$ $\beta^{+}EC$ and 2$\nu$ $ECEC$ for $^{124,126}$Xe and $^{130,132}$Ba nuclei are presented. Calculated quadrupolar transition probabilities B(E2: $0^+\to 2^+$), static quadrupole moments and $g$ factors in the parent and daughter nuclei reproduce the experimental information, validating the reliability of the model wave functions. The anticorrelation between nuclear deformation and the nuclear transition matrix element $M_{2\nu}$ is confirmed.Comment: 19 page

Fusarium oxysporum f. sp. lycopersici causal agent of vascular wilt disease of tomato: Biology to diversity– A review

Tomato (Lycopersicon esculentum) is one of the widely grown vegetables worldwide. Fusarium oxysporum f. sp. lycopersici (FOL) is the significant contributory pathogen of tomato vascular wilt. The initial symptoms of the disease appear in the lower leaves gradually, trail by wilting of the plants. It has been reported that FOL penetrates the tomato plant, colonizing and leaving the vascular tissue dark brown, and this discoloration extends to the apex, leading to the plants wilting, collapsing and dying. Therefore, it has been widely accepted that wilting caused by this fungus is the result of a combination of various physiological activities, including the accumulation of fungal mycelia in and around xylem, mycotoxin production, inactivation of host defense, and the production of tyloses; however, wilting symptoms are variable. Therefore, the selection of molecular markers may be a more effective means of screening tomato races. Several studies on the detection of FOL have been carried out and have suggested the potency of the technique for diagnosing FOL. This review focuses on biology and variability of FOL, understanding and presenting a holistic picture of the vascular wilt disease of tomato in relation to disease model, biology, virulence. We conclude that genomic and proteomic approachesare greater tools for identification of informative candidates involved in pathogenicity, which can be considered as one of the approaches in managing the disease

Withaferin a-induced apoptosis in human breast cancer cells is mediated by reactive oxygen species

Withaferin A (WA), a promising anticancer constituent of Ayurvedic medicinal plant Withania somnifera, inhibits growth of MDA-MB-231 and MCF-7 human breast cancer cells in culture and MDA-MB-231 xenografts in vivo in association with apoptosis induction, but the mechanism of cell death is not fully understood. We now demonstrate, for the first time, that WA-induced apoptosis is mediated by reactive oxygen species (ROS) production due to inhibition of mitochondrial respiration. WA treatment caused ROS production in MDA-MB-231 and MCF-7 cells, but not in a normal human mammary epithelial cell line (HMEC). The HMEC was also resistant to WA-induced apoptosis. WA-mediated ROS production as well as apoptotic histone-associated DNA fragment release into the cytosol was significantly attenuated by ectopic expression of Cu,Zn-superoxide dismutase in both MDA-MB-231 and MCF-7 cells. ROS production resulting from WA exposure was accompanied by inhibition of oxidative phosphorylation and inhibition of complex III activity. Mitochondrial DNA-deficient Rho-0 variants of MDA-MB-231 and MCF-7 cells were resistant to WA-induced ROS production, collapse of mitochondrial membrane potential, and apoptosis compared with respective wild-type cells. WA treatment resulted in activation of Bax and Bak in MDA-MB-231 and MCF-7 cells, and SV40 immortalized embryonic fibroblasts derived from Bax and Bak double knockout mouse were significantly more resistant to WA-induced apoptosis compared with fibroblasts derived from wild-type mouse. In conclusion, the present study provides novel insight into the molecular circuitry of WA-induced apoptosis involving ROS production and activation of Bax/Bak. © 2011 Hahm et al

Aggregated a-synuclein and complex I deficiency: exploration of their relationship in differentiated neurons

α-Synuclein becomes misfolded and aggregated upon damage by various factors, for example, by reactive oxygen species. These aggregated forms have been proposed to have differential toxicities and their interaction with mitochondria may cause dysfunction within this organelle that contributes to the pathogenesis of Parkinson’s disease (PD). In particular, the association of α-synuclein with mitochondria occurs through interaction with mitochondrial complex I and importantly defects of this protein have been linked to the pathogenesis of PD. Therefore, we investigated the relationship between aggregated α-synuclein and mitochondrial dysfunction, and the consequences of this interaction on cell survival. To do this, we studied the effects of α-synuclein on cybrid cell lines harbouring mutations in either mitochondrial complex I or IV. We found that aggregated α-synuclein inhibited mitochondrial complex I in control and complex IV-deficient cells. However, when aggregated α-synuclein was applied to complex I-deficient cells, there was no additional inhibition of mitochondrial function or increase in cell death. This would suggest that as complex I-deficient cells have already adapted to their mitochondrial defect, the subsequent toxic effects of α-synuclein are reduced

Acquisition of Chemoresistance in Gliomas Is Associated with Increased Mitochondrial Coupling and Decreased ROS Production

Temozolomide (TMZ) is an alkylating agent used for treating gliomas. Chemoresistance is a severe limitation to TMZ therapy; there is a critical need to understand the underlying mechanisms that determine tumor response to TMZ. We recently reported that chemoresistance to TMZ is related to a remodeling of the entire electron transport chain, with significant increases in the activity of complexes II/III and cytochrome c oxidase (CcO). Moreover, pharmacologic and genetic manipulation of CcO reverses chemoresistance. Therefore, to test the hypothesis that TMZ-resistance arises from tighter mitochondrial coupling and decreased production of reactive oxygen species (ROS), we have assessed mitochondrial function in TMZ-sensitive and -resistant glioma cells, and in TMZ-resistant glioblastoma multiform (GBM) xenograft lines (xenolines). Maximum ADP-stimulated (state 3) rates of mitochondrial oxygen consumption were greater in TMZ-resistant cells and xenolines, and basal respiration (state 2), proton leak (state 4), and mitochondrial ROS production were significantly lower in TMZ-resistant cells. Furthermore, TMZ-resistant cells consumed less glucose and produced less lactic acid. Chemoresistant cells were insensitive to the oxidative stress induced by TMZ and hydrogen peroxide challenges, but treatment with the oxidant L-buthionine-S,R-sulfoximine increased TMZ-dependent ROS generation and reversed chemoresistance. Importantly, treatment with the antioxidant N-acetyl-cysteine inhibited TMZ-dependent ROS generation in chemosensitive cells, preventing TMZ toxicity. Finally, we found that mitochondrial DNA-depleted cells (ρ°) were resistant to TMZ and had lower intracellular ROS levels after TMZ exposure compared with parental cells. Repopulation of ρ° cells with mitochondria restored ROS production and sensitivity to TMZ. Taken together, our results indicate that chemoresistance to TMZ is linked to tighter mitochondrial coupling and low ROS production, and suggest a novel mitochondrial ROS-dependent mechanism underlying TMZ-chemoresistance in glioma. Thus, perturbation of mitochondrial functions and changes in redox status might constitute a novel strategy for sensitizing glioma cells to therapeutic approaches