Tomato Management Practices and Diseases Occurrence in Mwea West Sub County

Tomato is an important crop in Mwea West Sub County, Kirinyaga County, Kenya. A survey was carried out in the area to investigate tomato management practices, diseases and pests that hinder tomato production. The study endeavoured to establish farmers’ knowledge on fusarium wilt disease and root-knot nematodes and the methods used to control them. Data was collected from two hundred and eighteen randomly selected small holder producers who were equally distributed in the study area. Data collected included tomato management practices, diseases and pests that hinder production. Majority (85.3%) of the respondents were males while a few (14.7%) were female. The respondents (71.6%) indicated that tomato was the most important crop grown for income generation in the area. Most important varieties grown were cultivars, Safari, Kilele F1, Prosta F1 and Rio- Grande. Most important diseases affecting tomato crop were; early blight (Alternaria solani) and late blight (Phytophthora infestans), fungal wilts (Fusarium sp. Verticillium sp. Rhizoctonia sp.) and bacterial wilt (Ralstonia solanacearum). Plant parasitic nematodes and pests (thrips, aphids, spider mites) were also reported in the study area. There was a significant(P<0.05) association between the following variables; type of land owner and major use of land, type of land owner and cropping system, source of agricultural information and whether or not to apply pesticides into the soil. Farmers were quite knowledgeable about tomato farming as they had access to information from various sources; however there are still major gaps in knowledge especially on diseases and pests. Keywords: Tomato, diseases, pests, nematodes, managemen

Stabilizing entanglement autonomously between two superconducting qubits

Quantum error-correction codes would protect an arbitrary state of a multi-qubit register against decoherence-induced errors, but their implementation is an outstanding challenge for the development of large-scale quantum computers. A first step is to stabilize a non-equilibrium state of a simple quantum system such as a qubit or a cavity mode in the presence of decoherence. Several groups have recently accomplished this goal using measurement-based feedback schemes. A next step is to prepare and stabilize a state of a composite system. Here we demonstrate the stabilization of an entangled Bell state of a quantum register of two superconducting qubits for an arbitrary time. Our result is achieved by an autonomous feedback scheme which combines continuous drives along with a specifically engineered coupling between the two-qubit register and a dissipative reservoir. Similar autonomous feedback techniques have recently been used for qubit reset and the stabilization of a single qubit state, as well as for creating and stabilizing states of multipartite quantum systems. Unlike conventional, measurement-based schemes, an autonomous approach counter-intuitively uses engineered dissipation to fight decoherence, obviating the need for a complicated external feedback loop to correct errors, simplifying implementation. Instead the feedback loop is built into the Hamiltonian such that the steady state of the system in the presence of drives and dissipation is a Bell state, an essential building-block state for quantum information processing. Such autonomous schemes, broadly applicable to a variety of physical systems as demonstrated by a concurrent publication with trapped ion qubits, will be an essential tool for the implementation of quantum-error correction.Comment: 39 pages, 7 figure

A Spectroscopic Study of Type Ibc Supernova Host Galaxies from Untargeted Surveys

We present the largest spectroscopic study of the host environments of Type Ibc supernovae (SN Ibc) discovered exclusively by untargeted SN searches. Past studies of SN Ibc host environments have been biased towards high-mass, high-metallicity galaxies by focusing on SNe discovered in galaxy-targeted SN searches. Our new observations more than double the total number of spectroscopic stellar population age and metallicity measurements published for untargeted SN Ibc host environments, and extend to a median redshift about twice as large as previous statistical studies (z = 0.04). For the 12 SNe Ib and 21 SNe Ic in our metallicity sample, we find median metallicities of log(O/H)+12 = 8.48 and 8.61, respectively, but determine that the discrepancy in the full distribution of metallicities is not statistically significant. This median difference would correspond to only a small difference in the mass loss via metal-line driven winds (<30%), suggesting this does not play the dominant role in distinguishing SN Ib and Ic progenitors. However, the median metallicity of the 7 broad-lined SN Ic (SN Ic-BL) in our sample is significantly lower, log(O/H)+12 = 8.34. The age of the young stellar population of SN Ic-BL host environments also seems to be lower than for SN Ib and Ic, but our age sample is small. A synthesis of SN Ibc host environment spectroscopy to date does not reveal a significant difference in SN Ib and Ic metallicities, but reinforces the significance of the lower metallicities for SN Ic-BL. This combined sample demonstrates that galaxy-targeted SN searches introduce a significant bias for studies seeking to infer the metallicity distribution of SN progenitors, and we identify and discuss other systematic effects that play smaller roles. We discuss the path forward for making progress on SN Ibc progenitor studies in the LSST era.Comment: 27 pages, 12 Figures, V2 as accepted by ApJ, more information at http://www.cfa.harvard.edu/~nsanders/papers/Ibchosts/summary.htm

Diamond Blackfan anemia is mediated by hyperactive Nemo-like kinase

Diamond Blackfan Anemia (DBA) is a congenital bone marrow failure syndrome associated with ribosomal gene mutations that lead to ribosomal insufficiency. DBA is characterized by anemia, congenital anomalies, and cancer predisposition. Treatment for DBA is associated with significant morbidity. Here, we report the identification of Nemo-like kinase (NLK) as a potential target for DBA therapy. To identify new DBA targets, we screen for small molecules that increase erythroid expansion in mouse models of DBA. This screen identified a compound that inhibits NLK. Chemical and genetic inhibition of NLK increases erythroid expansion in mouse and human progenitors, including bone marrow cells from DBA patients. In DBA models and patient samples, aberrant NLK activation is initiated at the Megakaryocyte/Erythroid Progenitor (MEP) stage of differentiation and is not observed in non-erythroid hematopoietic lineages or healthy erythroblasts. We propose that NLK mediates aberrant erythropoiesis in DBA and is a potential target for therapy

Activation of tumor suppressor protein PP2A inhibits KRAS-driven tumor growth

Targeted cancer therapies, which act on specific cancer-associated molecular targets, are predominantly inhibitors of oncogenic kinases. While these drugs have achieved some clinical success, the inactivation of kinase signaling via stimulation of endogenous phosphatases has received minimal attention as an alternative targeted approach. Here, we have demonstrated that activation of the tumor suppressor protein phosphatase 2A (PP2A), a negative regulator of multiple oncogenic signaling proteins, is a promising therapeutic approach for the treatment of cancers. Our group previously developed a series of orally bioavailable small molecule activators of PP2A, termed SMAPs. We now report that SMAP treatment inhibited the growth of KRAS-mutant lung cancers in mouse xenografts and transgenic models. Mechanistically, we found that SMAPs act by binding to the PP2A Aα scaffold subunit to drive conformational changes in PP2A. These results show that PP2A can be activated in cancer cells to inhibit proliferation. Our strategy of reactivating endogenous PP2A may be applicable to the treatment of other diseases and represents an advancement toward the development of small molecule activators of tumor suppressor proteins

Deletion of a Malaria Invasion Gene Reduces Death and Anemia, in Model Hosts

Malaria parasites induce complex cellular and clinical phenotypes, including anemia, cerebral malaria and death in a wide range of mammalian hosts. Host genes and parasite ‘toxins’ have been implicated in malarial disease, but the contribution of parasite genes remains to be fully defined. Here we assess disease in BALB/c mice and Wistar rats infected by the rodent malaria parasite Plasmodium berghei with a gene knock out for merozoite surface protein (MSP) 7. MSP7 is not essential for infection but in P. falciparum, it enhances erythrocyte invasion by 20%. In vivo, as compared to wild type, the P. berghei Δmsp7 mutant is associated with an abrogation of death and a decrease from 3% to 2% in peak, circulating parasitemia. The Δmsp7 mutant is also associated with less anemia and modest increase in the size of follicles in the spleen. Together these data show that deletion of a single parasite invasion ligand modulates blood stage disease, as measured by death and anemia. This work is the first to assess the contribution of a gene present in all plasmodial species in severe disease

Krüppel-Like Factor 6 Expression Changes during Trophoblast Syncytialization and Transactivates ßhCG and PSG Placental Genes

BACKGROUND: Krüppel-like factor-6 (KLF6) is a widely expressed member of the Sp1/KLF family of transcriptional regulators involved in differentiation, cell cycle control and proliferation in several cell systems. Even though the highest expression level of KLF6 has been detected in human and mice placenta, its function in trophoblast physiology is still unknown. METHODOLOGY/PRINCIPAL FINDINGS: Herein, we explored KLF6 expression and sub-cellular distribution in human trophoblast cells differentiating into the syncytial pathway, and its role in the regulation of genes associated with placental development and pregnancy maintenance. Confocal immunofluorescence microscopy demonstrated that KLF6 is expressed throughout human cytotrophoblast differentiation showing no evident modifications in its nuclear and cytoplasmic localization pattern. KLF6 transcript and protein peaked early during the syncytialization process as determined by qRT-PCR and western blot assays. Overexpression of KLF6 in trophoblast-derived JEG-3 cells showed a preferential nuclear signal correlating with enhanced expression of human β-chorionic gonadotropin (βhCG) and pregnancy-specific glycoprotein (PSG) genes. Moreover, KLF6 transactivated βhCG5, PSG5 and PSG3 gene promoters. Deletion of KLF6 Zn-finger DNA binding domain or mutation of the consensus KLF6 binding site abolished transactivation of the PSG5 promoter. CONCLUSIONS/SIGNIFICANCE: Results are consistent with KLF6 playing a role as transcriptional regulator of relevant genes for placental differentiation and physiology such as βhCG and PSG, in agreement with an early and transient increase of KLF6 expression during trophoblast syncytialization