Phytochemical screening and antifungal activity of sawdust and stem bark extracts from Erythrophleum suaveolens (Guill. & Perr) Brena

This study was carried out to investigate the antifungal potentials of stem bark and sawdust of Erythrophleum suaveolens. Stem bark was collected from Federal University of Agriculture (FUAM) while sawdust sample was collected from Timber Shed Makurdi. Both samples were air dried while the stem bark was ground into powder for extraction. Extraction of samples was done sequentially by macerating 1000 g and 600 g of stem bark and sawdust, respectively using 1000 mL (w/v) of n-hexane for 24 hours and filtering off the hexane extract followed by ethyl acetate and methanol in that order for 24 hours each. Extracts were filtered and evaporated to obtain dried extracts and yields calculated. Phytochemical screening of samples was carried out according to AOAC standard methods. Diffusion method was used for antifungal screening of extracts. Sabouraud Dextrose agar was prepared as media in Petri dishes where Zones of Inhibition were observed for fungal growth. Minimum Inhibitory Concentration (MIC) of extracts was determined according to broth dilution technique at 40 g/mL, 20 g/mL, 10 g/mL, 5 g/mL and 2.5 g/mL. Minimum Fungicidal Concentration (MFC) determined by sub culturing MIC to determine the least concentration at which fungi were killed. Percentage yield of extract was highest (5.19 %) in stem bark and lowest (0.12 %) in sawdust. Methanol extracts had the highest yield (5.19 % and 3.42 %) for stem bark and sawdust followed by ethyl acetate (1.06 % and 0.36 %) and n’ hexane (0.16 % and 0.12 %), respectively. Flavonoids, glycosides, saponins, steroids, and tannins were in the stem bark while, anthraquinones, saponins and tannins were completely absent in the E. suaveolens sawdust. Zones of Inhibition (ZOIs) of antibiotics ranged between 27 mm – 35 mm while ZOIs for crude extracts ranged from 18 mm – 28 mm. At MIC of 5 mg/mL, E. Suaveolens stem bark methanol extract inhibited Coniophora puteana and Fomitopsis pinicoca growth. At MFC of 10 mg/mL the same microbes were killed. Erythrophleum suaveolens stem bark methanol can be used in the control of brown-rot decay and stem decay caused by Coniophora puteana and Fomitopsis pinicoca.Keywords: Antifungal, brown-rot decay, stem decay, Erythrophleum suaveolens, Coniophora puteana, Fomitopsis pinicoca, Antimicrobial, Aspergillus fumigatu

Transient inter-cellular polymeric linker

10.1016/j.biomaterials.2007.04.034Biomaterials28253656-366

The association between murine cytomegalovirus induced hepatitis and the accummulation of oval cells

The accumulation of oval cells is an early event in the development of hepatocellular carcinoma induced by certain experimental regimes involving hepatocarcinogens. Oval cells have also been observed during chronic hepatitis induced by alcohol and iron overload. In this study, livers of murine cytomegalovirus (MCMV) infected mice were examined to determine whether hepatitis induced by this virus could initiate oval cell proliferation. BALB/c and C57BL/6 mice were infected with MCMV and studied 4, 8, 10 and 12 months later, alongside control (uninfected) mice. The livers were examined histochemically, immunocytochemically and by in situ hybridization to identify oval cells, inflammatory cells and proliferating cells. Oval cells were seen in the periportal regions of livers from MCMV infected BALB/c mice. These increased in number from 4 to 12 months after infection in parallel with increases in the numbers of inflammatory cells, even though cells expressing MCMV antigens were no longer evident in these samples. Proliferating oval cells and hepatocytes were identified by PCNA staining, indicating an increased level of liver regeneration in the infected livers. C57BL/6 mice are less susceptible to persistent MCMV hepatitis and had fewer oval cells than BALB/c mice. Thus the study demonstrates an association between MCMV induced hepatitis, inflammation, and presence of oval cells

Landscape of somatic mutations in 560 breast cancer whole-genome sequences

We analysed whole-genome sequences of 560 breast cancers to advance understanding of the driver mutations conferring clonal advantage and the mutational processes generating somatic mutations. We found that 93 protein-coding cancer genes carried probable driver mutations. Some non-coding regions exhibited high mutation frequencies, but most have distinctive structural features probably causing elevated mutation rates and do not contain driver mutations. Mutational signature analysis was extended to genome rearrangements and revealed twelve base substitution and six rearrangement signatures. Three rearrangement signatures, characterized by tandem duplications or deletions, appear associated with defective homologous-recombination-based DNA repair: one with deficient BRCA1 function, another with deficient BRCA1 or BRCA2 function, the cause of the third is unknown. This analysis of all classes of somatic mutation across exons, introns and intergenic regions highlights the repertoire of cancer genes and mutational processes operating, and progresses towards a comprehensive account of the somatic genetic basis of breast cancer