Eight selective nitrogen-sulfur donor ligands have been synthesized from the condensation of S-methyldithiocarbazate (SMDTC) with aldehydes and ketones with a view to evaluating their antimicrobial and cytotoxic activities, and also to correlate the biological properties with the structure of the ligands. The compounds were all characterized by elemental analyses and other physicochemical techniques. SMDTC and the Schiff bases were screened for antimicrobial and cytotoxic activities. SMDTC showed very large inhibition zones (24-44 mm) against bacteria and fungi with a minimum inhibitory concentration (MIC) of 390-25,000 and 1562-6250 microg ml(-1), against different bacteria and fungi, respectively. Streptomycin and nystatin were used as the internal standards against bacteria and fungi, respectively. SMDTC along with its Schiff bases with pyridine-2-carboxaldehyde, acetylacetone and 2,3-butanedione were strongly antifungal and the MIC values were comparable to nystatin. Most of the Schiff bases were strongly cytotoxic. In particular, those with pyridine-2-carboxaldehyde and 2,3-butanedione have CD(50) values of 5.5, 1.9-2.0 microg ml(-1), respectively, against leukemic cells, while against colon cancer cells, the values were 3.7 and 2.0 microg ml(-1), respectively. The glyoxal Schiff base was strongly active only against leukemic cell with CD(50) value of 4.0 microg ml(-1). The present findings have been compared with standard drugs.

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Mungbean is one of the most important pulse crops in Bangladesh. The demand of mungbean is very high due to its good taste. To date, different national institutes released 14 improve mungbean varieties with complete package of technologies and disseminated them to the farmers. But, the farm level adoption of mungbean varieties, their economics, and farmer’s efficiencies are not well known to the researchers and policy planners. Therefore, the study assessed the farm level adoption of mungbean technologies, technical efficiency of mungbean growers, and find out constraints to its higher production. Data were collected from 283 randomly selected mungbean farmers from Jessore, Kushtia, and Barisal districts during March-April 2009. The highly adopted mungbean varieties were BARI Mung-3, 4 and 5. Technologies, such as ploughing, weeding, and seed rate occupied higher level of adoption. Sowing time and insect-pest control were medium level and irrigation was lower level adoption. In case of chemical fertilizer, urea secured higher level of adoption followed by TSP and MoP. The yield and net return of mungbean was 1196 kg and Tk. 15678 per hectare, respectively. The benefit cost ratio was 1.69 and 2.47 on full cost and cash cost basis, respectively. About 67% farmers achieved more than 90% technical efficiency level. Twenty eight percent farmers’ technical efficiency level, between 81-90% and the rest 5% farmers’ technical efficiency level was less than 80%. Diseases and pest infestation, lack of good quality seed, lack of knowledge about improved technologies were the major constraints to mungbean cultivation. Government should provide hand-on training and distribute quality seed to the farmers for increasing the area of mungbean cultivation. DOI: http://dx.doi.org/10.3329/bjar.v39i1.20149 Bangladesh J. Agril. Res. 39(1): 113-125, March 2014

SF3B1 is the most frequently mutated RNA splicing factor in multiple neoplasms, including ~25% of myelodysplastic syndromes (MDS) patients. Mortality in MDS frequently results from severe anemia, but the underlying mechanism is largely unknown. Here we elucidate the detailed, elusive pathway by which SF3B1 mutations cause anemia. We demonstrate, in CRISPR-edited cell models, normal human primary cells, and MDS patient cells, that mutant SF3B1 induces a splicing error in transcripts encoding the kinase MAP3K7, resulting in reduced MAP3K7 protein levels and deactivation of downstream target p38 MAPK. We show that disruption of this MAP3K7-p38 MAPK pathway leads to premature downregulation of GATA1, a master regulator of erythroid differentiation, and that this is sufficient to trigger accelerated differentiation and apoptosis. As a result, the overproduced, late staged erythroblasts undergo apoptosis and are unable to mature in the bone marrow. Our findings provide a detailed mechanism explaining the origins of anemia in MDS patients harboring SF3B1 mutations.In an effort to elucidate the functions of mutant SF3B1, knock-in mice carrying the most common hotspot mutation in MDS, K700E, were generated17,18. These mice displayed erythroid dysplasia, but were not able to recapitulate other cardinal features of MDS, particularly RARS phenotypes such as accumulation of erythroid precursors in the bone marrow, increased apoptotic bone marrow cells or erythroid precursors, and appearance of ringed sideroblasts5,7,8,19-22 . In addition, there was very little overlap of misspliced transcripts between MDS patients and the mutant mice (~ 5-10%, 17; 18), most likely due to the poor conservation of intronic sequences (~30%) between human and mouse23 and significant differences in alternative splicing24. Thus, the very little overlap of misspliced gene transcripts between MDS patients and mutant mice questions whether the observed erythroid dysplasia is a mouse-specific effect. Hence, while mutant mouse models can be valuable, they may be less useful in modeling splicing-related diseases such as MDS.Numerous aberrantly spliced transcripts have been identified in SF3B1 mutant samples obtained from MDS patients. However, very few of these have been shown to contribute to MDS phenotypes. Recently, it was reported that missplicing of the transcript encoding the erythroid hormone erythroferrone, and the resultant decreased levels of the hormone, might be responsible for the systemic iron loading seen in MDS patients with SF3B1 mutations who had not received blood transfusions25. In addition, missplicing of the transcript encoding the mitochondrial ATPbinding cassette iron transporter ABCB7 induced by mutant SF3B1 may be responsible for the accumulation of ring sideroblasts in MDS26,27. Despite these important insights into the identity of key mutant SF3B1 target gene transcripts, the mechanism by which SF3B1 mutations induce anemia in MDS patients is unknown.