LL-A491, A Monazomycin-like Antibiotic

A new antibiotic, designated LL-A491, was isolated by butanol extraction and crystallization from beers of an unidentified streptomycete, Lederle culture A491. LL-A491 was primarily active against gram-positive bacteria and was related to monazomycin. A tentative molecular formula of C_72±2 H_144±8 O_25±1 N for the antibiotic, based on analyses of the crystalline hydrochloride, picrate, and picrolonate salts, is considerably larger than that proposed for monazomycin, from which LL-A491 was not differentiated by paper chromatography. Analysis of the amorphous polyacetate ester suggested 15 to 16 acetylable groups. Upon hydrolysis, LL-A491 liberated ammonia and a reducing sugar which appeared to be mannose. LL-A491 was dextrorotatory, [α]_D²⁵ + 14°, and exhibited only end absorption in the ultraviolet region.     

Shifting in the duplication time of sex chromosomes in the rat

Duplication of sex chromosomes was studied in bone marrow cells from adult rats and in short-term cultures of rat fetus cells. Results obtained indicate that: a) G₂ period takes 4 hours in cells from fetuses and 3 hours in bone marrow cells, b) S period lasts 7 hours in bone marrow cells and about 20 hours in short-term cultured cells from fetuses, c) In cells from female fetuses one X-chromosome is the last to start DNA synthesis and also one of the X's is the last to end replication, d) In cells from female adult rats both X-chromosomes start and finish DNA synthesis early, e) In both line of cells the Y-chromosome was the last to begin and the last to finish DNA synthesis. — Causes which can account for the differences between the two line of cells are discussed.     

Differential induction of type I interferon responses in myeloid dendritic cells by mosquito and mammalian-cell-derived alphaviruses

Dendritic cells (DCs) are an important early target cell for many mosquito-borne viruses, and in many cases mosquito-cell-derived arboviruses more efficiently infect DCs than viruses derived from mammalian cells. However, whether mosquito-cell-derived viruses differ from mammalian-cell-derived viruses in their ability to induce antiviral responses in the infected dendritic cell has not been evaluated. In this report, alphaviruses, which are mosquito-borne viruses that cause diseases ranging from encephalitis to arthritis, were used to determine whether viruses grown in mosquito cells differed from mammalian-cell-derived viruses in their ability to induce type I interferon (IFN) responses in infected primary dendritic cells. Consistent with previous results, mosquito-cell-derived Ross River virus (mos-RRV) and Venezuelan equine encephalitis virus (mos-VEE) exhibited enhanced infection of primary myeloid dendritic cells (mDCs) compared to mammalian-cell-derived virus preparations. However, unlike the mammalian-cell-derived viruses, which induced high levels of type I IFN in the infected mDC cultures, mos-RRV and mos-VEE were poor IFN inducers. Furthermore, the poor IFN induction by mos-RRV contributed to the enhanced infection of mDCs by mos-RRV. These results suggest that the viruses initially delivered by the mosquito vector differ from those generated in subsequent rounds of replication in the host, not just with respect to their ability to infect dendritic cells but also in their ability to induce or inhibit antiviral type I IFN responses. This difference may have an important impact on the mosquito-borne virus's ability to successfully make the transition from the arthropod vector to the vertebrate host.     

Fish determine macroinvertebrate food webs and assemblage structure in Greenland subarctic streams

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A model for genetic complementation controlling the chromosomal abnormalities and loss of heterozygosity formation in cancer

The relationship between the apparently random chromosomal changes found in aneuploidy and the genetic instability driving the progression of cancer is not clear. We report a test of the hypothesis that aneuploid chromosomal abnormalities might be selected to preserve cell-survival genes during loss of heterozygosity (LOH) formations which eliminate tumor suppressor genes. The LOHs and structurally abnormal chromosomes present in the aneuploid LoVo (colon), A549 (lung), SUIT-2 (pancreas), and LN-18 (glioma) cancer cell lines were identified by single nucleotide polymorphisms (SNPs) and Spectral Karyotyping (SKY). The Mann-Whitney U and chi square tests were used to evaluate possible differences in chromosome numbers and abnormalities between the cell lines, with two-tailed P values of <0.01 being considered significant. The cell lines differed significantly in chromosome numbers and frequency of structurally abnormal chromosomes. The SNP analysis revealed that each cell line contained at least a haploid set of somatic chromosomes, consistent with our hypothesis that cell-survival genes are widely scattered throughout the genome. Further, over 90% of the chromosomal abnormalities seemed to be selected, often after LOH formation, for gene-dosage compensation or to provide heterozygosity for specific chromosomal regions. These results suggest that the chromosomal changes of aneuploidy are not random, but may be selected to provide gene-dosage compensation and/or retain functional alleles of cell-survival genes during LOH formation.     

Variation in the Distribution of Trace Elements in Renal Cell Carcinoma

The development of cancer is a complex, multistage process during which a normal cell undergoes genetic changes that result in phenotypic alterations and in the acquisition of the ability to invade other sites. Inductively coupled plasma optical emission spectroscopy was used to estimate the contents of Al, Ca, Cd, Cr, Cu, Fe, K, Mg, Mn, Na, P, Pb, and Zn in healthy kidney and renal cell carcinoma (RCC), and significant differences were found for all elements. Along with the progression of the malignant disease, a progressive decrease of Cd and K was observed. In fact, for Cd, the concentration in stage T4 was 263.9 times lower than in stage T1, and for K, the concentration in stage T4 was 1.73 times lower than in stage T1. Progressive accumulation was detected for P, Pb, and Zn in stage T4. For P, the concentration in stage T4 was 11.1 times higher than in stage T1; for Pb, the concentration in stage T4 was 232.7 times higher than in T1; and for Zn, the concentration in T4 was 8.452 times higher than in T1. This study highlights the marked differences in the concentrations of selected trace metals in different malignant tumor stages. These findings indicate that some trace metals may play important roles in the pathogenesis of RCC.