Radioprotective action of a combination of poly I-poly C and mexamine

In experiments on (CBA X C57Bl)F1 mice irradiated with doses of 8-12 Gy a study was made of the effect of a mixture of polyI-polyC (2.5 mg/kg, 2 days before irradiation) and mexamine (30 mg/kg, 5 min before irradiation) on the survival rate of animals and the times of their death. It was shown that polyI-polyC potentiates the protective effect of mexamine not increasing its toxicity. The protective agents used in a combination decrease the "intestinal" death of irradiated animals while used separately fail to produce this effect.     

Lack of correlation between the lifetimes of mRNA and the initial lengths of their poly a segments

Molecular Biology Reports - In mouse liver polyribosomes two poly A-containing messenger RNA species have been found: a short-lived one with a lifetime of 1 to 1.5 hr in the free polyribosomes and...     

Effect of concanavalin A on interferon induction by poly IC

Concanavalin A, a plant lectin having specific membrane properties, has an inhibitory effect on interferon induction by poly IC, both in human fibroblast and mouse 3T3 cells. In the studied systems, the inhibition is independent of an effect on polynucleotide binding.     

Inverse correlation between bacterial frameshift mutagenicity and yeast mitochondrial effects of antitumour anilinoacridines

The mutagenicity of a series of derivatives of 9-anilinoacridine, including the clinical antitumour agent amsacrine, has been assessed using a bacterial frameshift tester strain (Salmonella typhimurium TA1537) and a yeast petite colony assay (Saccharomyces cerevisiae 5178B). The results have been compared with microbial mammalian cell cytotoxicity, DNA binding affinity and acridine base strength (pKa). Compounds containing strong electron donor substituents on the acridine ring, and which have a high acridine pKa, show minimal frameshift mutagenicity but are strong inducers of petite yeast mutants. Conversely, some compounds which have a high DNA binding constant but a significant proportion of uncharged form at neutral pH, show high frameshift mutagenicity but minimal induction of petite mutants. It is hypothesised that this inverse relationship arises from the presence of trans-membrane drug transport mechanisms which act to exclude some compounds, particularly strongly basic compounds from the cytoplasm and to concentrate them in mitochondria.     

Lack of correlation between aristolochic acid exposure and hepatocellular carcinoma

正Besides upper tract urothelial cell carcinoma(UTUCs),a recent study published in Science Translational Medicine has indicated that liver cancer may be associated with the exposure of aristolochic acids and similar derivatives(collectively,AA).However,according to our research,this study needs more number of samples for further verification which should be sampled from a wider range of people.     

Lack of correlation between ultrastructural and pharmacological types of non-adrenergic autonomic nerves

Summary In order to test the premise that non-adrenergic, non-cholinergic (NANC) autonomic nerves have a distinctive ultrastructural appearance, clearly different from that of cholinergic nerves, a detailed quantitative ultrastructural analysis has been made of the non-adrenergic innervation of 15 tissues thought from pharmacological evidence to be innervated by NANC nerves (rat and rabbit anococcygeus muscles; rabbit hepatic portal vein; extrinsically denervated toad lung); cholinergic nerves (atria of rat, rabbit, guinea-pig and toad); or both (guinea-pig cervical and thoracic trachealis muscle; rabbit rectococcygeus muscle; urinary bladder of rat, rabbit, guinea-pig and toad) in addition to their adrenergic supply. Following fixation with a modified chromaffin procedure allowing identification of adrenergic nerves, large, randomly selected samples of non-adrenergic nerve profiles from each tissue were analysed with respect to numbers, relative proportions, and size frequency distributions of different vesicle classes within the profiles. The neuromuscular relationships within each tissue were also analysed. On the basis of these analyses, it is clear that there are no consistent ultrastructural differences between cholinergic and NANC autonomic nerves: neither proportions nor sizes of the vesicles provide any clue as to the transmitter used by a particular nerve. The great majority of nerve profiles, whether cholinergic or NANC, contain predominantly small clear synaptic vesicles. Large filled peptidergic vesicles are no more common in most NANC nerves than in most cholinergic ones. It is concluded, on ultrastructural grounds, that the primary transmitter in these NANC autonomie nerves is most likely to be stored in and released from the small clear vesicles.     

Proteins induced by the double-stranded interferon inducer poly(I).poly(C)

The possible pathways for realization of antiviral activity of interferon inducer poly (I).poly(C) have been studied. The stimulating effect of interferon inducer on the net protein synthesis in human M19 fibroblasts has been demonstrated. Compositions of the specific proteins induced by poly(I).poly(C) or interferon in human M19 fibroblasts and in monkey cells 4647 have been analyzed by electrophoresis technique. The data obtained suggest the existence of common gene products for interferon and ds-inducer. The ds-inducer requires the synthesis of lesser amounts of proteins for realization of its biological activity as compared with interferon.     

Lack of correlation between cytotoxic T lymphocytes and lethal murine lymphocytic choriomeningitis

Adoptive transfer of lymph node and spleen cells from mice infected with LCM virus to similarly infected immunocompromised recipients has been the classic way to demonstrate the lethal role of T cells in the CNS disease caused by this virus. Isolation and adoptive transfer techniques are presented here which show that Thy-1+ cells isolated from the meningeal infiltrates (MI) of LCM virus-infected mice possess this property. We compared various T cell functions of MI cells taken from mice infected with two strains of LCM virus differing markedly in their pathogenicities. One of these strains, termed aggressive, caused a typical, invariably fatal, CNS disease within 7 to 10 days after infection. The other virus, termed docile, killed few mice after the standard intracerebral inoculation, and could persist in the mice for 6 mo or more. The yields of MI leukocytes from mice infected with docile virus varied from 50 to 100% of those found in mice infected with aggressive virus (3 X 10(6) cells/brain). On a cell-to-cell basis, the CTL activity in the MI of mice infected with docile virus ranged from 50 to 100% of that found in the MI of mice infected with aggressive virus. MI cells from mice infected with aggressive virus consistently caused lethal disease by adoptive transfer into immunocompromised (irradiated) recipients infected with either strain of virus. All attempts to induce lethal disease by adoptive transfer of MI cells (or splenocytes) from mice infected with docile virus into irradiated recipients failed. The latter experiments with the docile-MI cells were performed with six times the number of aggressive-MI cells needed to kill irradiated recipients by adoptive transfer. The possible reasons for this discordance between CTL and in vivo killer function are discussed.     

Oxytocin action: Lack of correlation between receptor number and tissue responsiveness

Brattleboro rats exhibit diabetes insipidus (DI) because of a genetic autosomal recessive defect in the synthesis of vasopressin; oxytocin is synthesized normally. Preliminary work suggests that elevated circulating oxytocin levels may compensate for the absence of vasopressin. To evaluate the consequences of presumed elevations of oxytocin levels, oxytocin binding and tissue responsiveness have been measured in the uterus and epididymal fat cells of homozygous-DI (HoDI) and heterozygous-DI (HeDI) animals and Sprague-Dawley and Long-Evans controls. Surprisingly, whereas membranes from HoDI rat uteri exhibited an 85% reduction in oxytocin binding, the biological response (contraction) to oxytocin was indistinguishable from the uteri of HeDI or Sprague-Dawley animals. The uterine response to carbachol was also normal in HoDI rats. In contrast, in adipocytes from HoDI animals, the biological response to oxytocin (glucose oxidation) was abolished, whereas the binding of oxytocin was normal; insulin-stimulated glucose oxidation was, however, normal. These results indicate that receptor binding, while critical to hormone action, is not the sole determining factor. With oxytocin action, postreceptor mechanisms are most important in determining oxytocin responsiveness.     

Lack of correlation between mutagen-induced chromosomal univalency and aneuploidy in mouse spermatocytes

Aneuploidy represents the predominant type of chromosomal abnormality found in human newborns with birth defects. The concern that environmental agents may cause aneuploidy in germ cells has prompted development of assay systems for detection of potentially aneuploidy-producing agents. One of the most frequently used methods involves cytogenetic analysis of murine spermatogenic cells at the stages of meiotic metaphases. However, criteria for aneuploidy induction have not been standardized in this test system. Many investigators consider the ability of an agent to induce univalents an appropriate measure of its potential to induce aneuploidy. In the present study, the relationship between univalency and aneuploidy was examined in mouse spermatocytes after various mutagen treatments. 45 Swiss mice were treated with 4 different agents; viz., adriamycin vinblastine sulfate, cytosine arabinoside, and radiation (cobalt 60) and 10 untreated animals served as controls. From each animal, 50–200 MIs were examined for both sex-chromosomal and autosomal univalency (X-Y U and AU), and equal numbers of MIIs were examined for aneuploidy (hyperhaploidy). No significant correlations between univalency (either X-Y U or AU) and aneuploidy were found in the mutagen-treated mice; nor were they found in the untreated animals. These results indicate that induction of univalents by a mutagen is not necessarily predictive of the aneuploidy-inducing ability of his agent.     

Lack of correlation between body mass and metabolic rate in Drosophila melanogaster

We examined the association between body mass and metabolic rate in Drosophila melanogaster under a variety of conditions. These included comparisons of body mass and metabolic rate in flies from different laboratory lines measured at different ages, over different metabolic sampling periods, and comparisons using wet versus dry mass data. In addition, the relationship between body mass and metabolic rate was determined for flies recently collected from wild populations. In no case was there a significant correlation between body mass and metabolic rate. These results indicate that care must be taken when attempting to account for the effects of body mass on metabolic rate. Expressing such data in mass-specific units may be an inappropriate method of attempting to control for the effects of differences in body mass.     

The effect of interferon induction on complement level in rat.

Relatively high levels of interferon were achieved in rat sera by intracardial inoculation with Sindbis virus followed 15 min later by intraperitoneal application of dimethylsulfoxide. At intervals when interferon titres reached the maximum, the levels of complement were decreased as compared with the control group of rats. Single administration of dimethylsulfoxide did neither induce interferon nor influence the complement levels in sera of rats of the Dobrá Voda breed tested. Similar results were obtained with concentrated Newcastle disease virus inoculated intraperitoneally. Of interest is the finding that properdin levels seem to increase at the same time as interferon.     

Lack of correlation between schistosomicidal and anticholinergic properties of hycanthone and related drugs

Visual observation of the motor activity of Schistosoma mansoni kept in vitro showed an increase of activity in the presence of hycanthone (HC). In addition, HC caused a delay in the paralytic effects of carbachol. Similar results were observed in the presence of oxamniquine (OXA). The same pattern of motor activity, however, was shown by HC-resistant worms, by Schistosoma japonicum, and by worms exposed to drug precursors (lucanthone and UK-3883), which are not schistosomicidal in vitro. Other analogs with in vitro killing activity (IA-4 and IA-4 N-oxide) showed minimal anticholinergic effects. The anticholinergic effects of HC and OXA were quickly reversible in vitro and in vivo, whereas their antischistosomal effects are irreversible and delayed. Incubation of schistosomes with high concentrations of carbachol or with anticholinergic drugs failed to compete with the schistosomicidal effects of HC. These results are viewed as contradictory to the hypothesis that HC kills schistosomes by blocking their acetylcholine receptors.