A highly conserved nuclear gene for low-level phylogenetics: elongation factor-1 alpha recovers morphology-based tree for heliothine moths

Molecular systematists need increased access to nuclear genes. Highly conserved, low copy number protein-encoding nuclear genes have attractive features for phylogenetic inference but have heretofore been applied mostly to very ancient divergences. By virtue of their synonymous substitutions, such genes should contain a wealth of information about lower-level taxonomic relationships as well, with the advantage that amino acid conservatism makes both alignment and primer definition straightforward. We tested this postulate for the elongation factor-1 alpha (EF-1 alpha) gene in the noctuid moth subfamily Heliothinae, which has probably diversified since the middle Tertiary. We sequenced 1,240 bp in 18 taxa representing heliothine groupings strongly supported by previous morphological and allozyme studies. The single most parsimonious gene tree and the neighbor-joining tree for all nucleotides show almost complete concordance with the morphological tree. Homoplasy and pairwise divergence levels are low, transition/transversion ratios are high, and phylogenetic information is spread evenly across gene regions. The EF-1 alpha gene and presumably other highly conserved genes hold much promise for phylogenetics of Tertiary age eukaryote groups.      

Adjustable metabolism units for swine

A swine metabolism unit was constructed which permitted separate quantitative collection of urine and feces. The unit was built of wood and proved to be reliable. It was adapted for studies with goats, sheep and young cattle.     

Effect of Glucose and CO(2) on Nitrate Uptake and Coupled OH Flux in Ankistrodesmus braunii

In Ankistrodesmus braunii, in the absence of CO₂, i.e. in CO₂-free air or N₂, photosynthetic nitrate uptake and nitrate reduction were inhibited, especially at low pH. Under such conditions, glucose stimulated nitrate uptake and reduction to almost the same level in the pH range between 6 and 8.5. CO₂ at 0.03% effected an intermediate pH dependence of nitrate uptake; saturating CO₂ concentration (more than 1%) eliminated the pH dependence, as did glucose, but the rates were enhanced compared with glucose. Glucose and, even more, CO₂, drastically reduced the release of nitrite and ammonia to the medium, the stoichiometry between alkalinization of the medium and nitrate uptake (OH⁻/NO₃⁻) approached 1.     

Androgen receptor complex binding in murine skeletal muscle nuclei

Examination of binding of androgen-receptor complexes from murine skeletal muscle cytosol was performed by modified nuclear retention assay and modified nuclear acceptor assay. The experiments showed the binding of androgen-receptor complexes to the nuclear acceptor sites to be a cooperative process. Hill analysis of the data obtained resulted in a Hill coefficient of 3,6. The apparent dissociation constant for binding of cytosolic [³H]-testosterone-receptor complexes to nuclei was found to be in the range of K_D = 6 ? 8 × 10^?11 M. The nuclear matrix was able to bind androgen-receptor complexes in a saturable way, too.     

Skeletal lesions and anemia associated with ascorbic acid deficiency in juvenile rhesus macaques.

Young rhesus macaques housed in outdoor corn cribs and fed a commercially prepared primate diet became weak, depressed, were reluctant to move, and expressed locomotor abnormalities. Thirteen severely affected animals were hospitalized for evaluation. Physical examination disclosed swellings and instabilities involving the ends of long bones. Radiography confirmed physeal fractures in 11 of 13 animals. Affected bones included the distal femur, proximal humerus, distal tibia/fibula, and distal radius/ulna. Other, less obvious changes were noted on radiographs. Anemia was a consistent finding. Ascorbic acid deficiency was suspected and therapy was initiated that consisted of vitamin supplements, diet change, cage rest, and support bandages. Feed samples were submitted to a laboratory for analysis and were confirmed deficient in vitamin C. Follow-up radiographs showed large calcifying subperiosteal hematomas in epiphyseometaphyseal regions, consistent with a diagnosis of scurvy. Twelve of 13 animals recovered clinically. Subsequent radiographs documented improvement of initially severe angular deformities associated with displaced fractures.     

Plant virus infection development as affected by heavy metal stress

The work was focused on the investigation of possible dependencies between the development of viral infection in plants and the presence of high heavy metal concentrations in soil. Field experiments have been conducted in order to study the development of systemic tobacco mosaic virus (TMV) infection in Lycopersicon esculentum L. cv. Miliana plants under effect of separate salts of heavy metals Cu, Zn and Pb deposited in soil. As it is shown, simultaneous effect of viral infection and heavy metals in tenfold maximum permissible concentration leads to decrease of total chlorophyll content in experiment plants mainly due to the degradation of chlorophyll a. The reduction of chlorophyll concentration under the combined influence of both stress factors was more serious comparing to the separate effect of every single factor. Plants' treatment with toxic concentrations of lead and zinc leaded to slight delay in the development of systemic TMV infection together with more than twofold increase of virus content in plants that may be an evidence of synergism between these heavy metal's and virus' effects. Contrary, copper although decreased total chlorophyll content but showed protective properties and significantly reduced amount of virus in plants.     

Evidence of Inbreeding in Hodgkin Lymphoma

Genome-wide association studies (GWASs) have identified several, mainly co-dominantly acting, single-nucleotide polymorphisms (SNPs) associated with Hodgkin lymphoma (HL). We searched for recessively acting disease loci by performing an analysis of runs of homozygosity (ROH) based on windows of homozygous SNP-blocks and by calculating genomic inbreeding coefficients on a SNP-wise basis. We used data from a previous GWAS with 906 cases and 1217 controls from a population with a long history of no matings between relatives. Ten recurrent ROHs were identified among 25 055 ROHs across all individuals but their association with HL was not genome-wide significant. All recurrent ROHs showed significant evidence for natural selection. As a novel finding genomic inbreeding among cases was significantly higher than among controls (P = 2.11*10⁻¹⁴) even after correcting for covariates. Higher inbreeding among the cases was mainly based on a group of individuals with a higher average length of ROHs per person. This result suggests a correlation of higher levels of inbreeding with higher cancer incidence and might reflect the existence of recessive alleles causing HL. Genomic inbreeding may result in a higher expression of deleterious recessive genes within a population.     

Liver cell death and anemia in Wilson disease involve acid sphingomyelinase and ceramide

Wilson disease is caused by accumulation of Cu(2+) in cells, which results in liver cirrhosis and, occasionally, anemia. Here, we show that Cu(2+) triggers hepatocyte apoptosis through activation of acid sphingomyelinase (Asm) and release of ceramide. Genetic deficiency or pharmacological inhibition of Asm prevented Cu(2+)-induced hepatocyte apoptosis and protected rats, genetically prone to develop Wilson disease, from acute hepatocyte death, liver failure and early death. Cu(2+) induced the secretion of activated Asm from leukocytes, leading to ceramide release in and phosphatidylserine exposure on erythrocytes, events also prevented by inhibition of Asm. Phosphatidylserine exposure resulted in immediate clearance of affected erythrocytes from the blood in mice. Accordingly, individuals with Wilson disease showed elevated plasma levels of Asm, and displayed a constitutive increase of ceramide- and phosphatidylserine-positive erythrocytes. Our data suggest a previously unidentified mechanism for liver cirrhosis and anemia in Wilson disease.