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Treatment options for patients with relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such as mutations in isocitrate dehydrogenase-1 and -2 (IDH1/2) are found in subsets of AML and MDS, are therapeutically targeted by mutant enzyme-specific small molecule inhibitors (IDH

A potential microalgal strain was isolated from dairy industrial effluent contaminated water and genetically identified as a close relative of Ascochloris sp. The current study demonstrates growth, biomass and lipid productivity of Ascochloris sp. ADW007 and simultaneous bioremediation of raw dairy waste water (RDW). Indoor microalgal cultivation studies were conducted in controlled conditions of light and temperature, while outdoor pilot-scale experiments were performed in errant conditions using semi-cylindrical barrel shaped open troughs. The rate of biomass productivity of ADW007 was improved with RDW as growth nutrient in indoor bench-scale (0.102 ± 0.003 g/L/d) and outdoor pilot-scale cultivations (0.207 ± 0.003 g/L/d) when compared with the algal growth in synthetic BG 11 medium (0.086 ± 0.004 g/L/d) and TAP medium (0.099 ± 0.003 g/L/d), respectively. Similarly, in outdoor conditions, the lipid content reached maximum to 34.98 ± 0.21% with volumetric and areal lipid productivities of 0.072 ± 0.001 g/L/d and 9.63 ± 0.08 g/m2/d, respectively. With this, the estimated annual algal oil production is nearly 20,495 ± 1953 gallons/acre/yr, if cultivated throughout the year. C18:0/C18:1 were the predominant fatty acids in lipid which indicates a great potential of ADW007 for biodiesel production and simultaneous bioremediation processes using RDW. Post-harvesting process includes hollow fiber filtration followed by activated carbon treatment and resulted in 95.1, 79.7 and 98.1% reduction in chemical oxygen demand, nitrate and total phosphate, respectively.

Normal organogenesis requires co-ordinate development and interaction of multiple cell types, and is seemingly governed by tissue specific factors. Lymphoid organogenesis during embryonic life is dependent on molecules the temporal expression of which is tightly regulated. During this process, haematopoietic 'inducer' cells interact with stromal 'organizer' cells, giving rise to the lymphoid organ primordia. Here we show that the haematopoietic cells in the gut exhibit a random pattern of motility before aggregation into the primordia of Peyer's patches, a major component of the gut-associated lymphoid tissue. We further show that a CD45+CD4-CD3-Il7Ralpha-c-Kit+CD11c+ haematopoietic population expressing lymphotoxin has an important role in the formation of Peyer's patches. A subset of these cells expresses the receptor tyrosine kinase RET, which is essential for mammalian enteric nervous system formation. We demonstrate that RET signalling is also crucial for Peyer's patch formation. Functional genetic analysis revealed that Gfra3-deficiency results in impairment of Peyer's patch development, suggesting that the signalling axis RET/GFRalpha3/ARTN is involved in this process. To support this hypothesis, we show that the RET ligand ARTN is a strong attractant of gut haematopoietic cells, inducing the formation of ectopic Peyer's patch-like structures. Our work strongly suggests that the RET signalling pathway, by regulating the development of both the nervous and lymphoid system in the gut, has a key role in the molecular mechanisms that orchestrate intestine organogenesis.

LEOPARD syndrome (lentigines, electrocardiographic conduction abnormalities, ocular hypertelorism, pulmonary stenosis, abnormal genitalia, retardation of growth, and sensorineural deafness) is an autosomal dominant condition. The main clinical features include multiple lentigines, cardiovascular defects, and facial anomalies, some of which are shared with Noonan syndrome (NS). Recent reports have shown that LEOPARD syndrome can be caused by mutations in PTPN11, the gene in which mutations can produce NS. Here we report the findings of mutation screening and linkage analysis of PTPN11 in three families with LEOPARD syndrome. We identified a novel mutation in one family. The mutation (1529A>C) substitutes proline for glutamine at amino acid 510 (Gln510Pro). No variations in sequence were observed in the other two families, and negative LOD scores excluded linkage to the PTPN11 locus, showing that LEOPARD syndrome is genetically heterogeneous.