Evaluation of the control of Myobia musculi infestations on laboratory mice with permethrin

The efficacy of permethrin against Myobia musculi (Schrank) (Acari:Myobiidae) infestations on mice was evaluated using four different dose delivery methods. In all methods, an attempt was made to deliver 0.5 mg of active permethrin weekly to each mouse. Successful control was achieved with topical or environmental treatment with 0.25% permethrin dust and by dipping the mice into a 0.6 g/l permethrin emulsion. The use of an emulsion applied to the bedding produced the least satisfactory control. Untreated mice had an average infestation rate of 57.3% throughout the study. No significant differences were seen between treated and untreated groups in either body weight or histopathology of the liver, lung, or kidney.     

2'-Nor-cGMP: a seco-cyclic nucleotide with powerful anti-DNA-viral activity

As part of our study of antiherpetic acyclonucleosides, we synthesized a cyclic GMP analog, 9-[(2-hydroxy-1,3,2-dioxaphosphorinan-5-yl)oxymethyl]guanine P-oxide, sodium salt (2'-nor-cGMP), and discovered its potent and broad spectrum anti-DNA-viral activities. 2'-Nor-cGMP inhibits the replication of many DNA viruses, including herpes simplex virus, human cytomegalovirus, vaccinia, SV40, and adenovirus, but does not inhibit RNA viruses. In plaque reduction studies this potent antiviral agent is also approximately 10-fold more potent than 9-(1,3-dihydroxy-2-propoxymethyl)guanine (2'NDG) against varicella-zoster virus and inhibits cell transformation by bovine papilloma virus. Unlike 2'NDG, the potent activity of 2'-nor-cGMP against herpes virus is not dependent upon the action of virus-specified thymidine kinase. Intercellular metabolism of 2'-nor-cGMP produced small amounts of 2'NDG triphosphate which were insufficient to account for the antiviral activity observed, implying that this potent anti-DNA-viral agent operates by a mechanism different from that of known acyclonucleosides.     

Effect of dopamine agonists or antagonists, TRH, stress and piglet removal on plasma prolactin concentrations in lactating gilts

The effect of dopamine agonists (ergocryptine), antagonists (chlorpromazine, haloperidol, reserpine, pimozide), thyrotropin releasing hormone or stress (restraint, piglet removal) on prolactin release was studied in primiparous lactating gilts. All animals were fitted with surgically implanted jugular catheters before farrowing. The only drug treatments which resulted in a significant change in PRL concentrations in blood were thyrotropin releasing hormone (increase) and ergocryptine (decrease). The results suggest that dopamine may not be the only regulator of prolactin in lactating pigs. Further studies are needed to identify drugs which would be useful in clinical situations for treatment of lactation failure due to low prolactin secretion. In the two stress-exposed groups, there was a gradual, steady decline in the plasma concentration of prolactin which resulted from loss of suckling contact with the piglets. Thus, snare restraint does not increase prolactin secretion in lactating sows confirming the results of other studies on pigs in different physiologic states.     

Analysis of a sequence region of 5S RNA from E. coli cross-linked in situ to the ribosomal protein L25.

70S ribosomes from E. coli were chemically cross-linked under conditions of in vitro protein biosynthesis. The ribosomal RNAs were extracted from reacted ribosomes and separated on sucrose gradients. The 5S RNA was shown to contain the ribosomal protein L25 covalently bound. After total RNase T1 hydrolysis of the covalent RNA-protein complex several high molecular weight RNA fragments were obtained and identified by sequencing. One fragment, sequence region U103 to U120, was shown to be directly linked to the protein first by protein specific staining of the particular fragment and second by phosphor cellulose chromatography of the covalent RNA-protein complex. The other two fragments, U89 to G106 and A34 to G51, could not be shown to be directly linked to L25 but were only formed under cross-linking conditions. While the fragment U89 to G106 may be protected from RNase T1 digestion because of a strong interaction with the covalent RNA-protein complex, the formation of the fragment A34 to G51 is very likely the result of a double monovalent modification of two neighbouring guanosines in the 5S RNA. The RNA sequences U103 to U120 established to be in direct contact to the protein L25 within the ribosome falls into the sequence region previously proposed as L25 binding site from studies with isolated 5S RNA-protein complexes.     

Regulation of substrate oxidation in isolated myocardial cells by beta-hydroxybutyrate

The role of ketone bodies in myocardial substrate oxidation was examined using freshly isolated Ca2+-tolerant heart myocytes, beta-hydroxybutyrate (beta OHB) inhibited lactate oxidation by the myocytes by 30-60%, and the inhibition was concentration dependent. Palmitate oxidation was also markedly decreased, whereas octanoate oxidation was only minimally affected by the presence of beta OHB. Lactate, octanoate, or palmitate had little, if any, effect on beta OHB oxidation. beta OHB oxidation was reduced by 22-28% in myocytes isolated from chronically diabetic rats, whereas the oxidation of palmitate remained similar to the controls. However, beta OHB still inhibited palmitate oxidation to the same extent as in the control cells. Our data support the role of beta OHB as a physiologic regulator of myocardial substrate metabolism.     

Immunoglobulin light chains in chronic lymphocytic leukemia and related diseases

The combination of two-dimensional mini gel electrophoresis with the 'western blot' technique proves to be a powerful tool in characterizing lymphoid cells. By testing for kappa and lambda immunoglobulin light chains we were able to differentiate between mono-, oligo-, and polyclonal B-cell diseases. The distribution of the lambda isotypes of 24 cases with chronic lymphocytic B-cell leukemia (B-CLL) tested was not random when compared to the distribution of the lambda light chains in B-lymphocytes of normal persons. This might implicate a genetic link between the lambda loci (chromosome 22) and the development of the lambda-CLL.     

Fatal myocarditis in mice fed rancid purified feed

An outbreak of disease characterized by diarrhea, severe myocarditis, and high mortality occurred in a group of 800 male B6C3F1/ Har mice fed powdered purified diets. A total of 292 animals died. No evidence of an infectious agent was found, and the disease was reproduced in healthy mice by feeding the purified diets, suggesting a nutritional deficiency or toxicity. Analysis of the feed revealed adequate levels of vitamin E, reduced levels of thiamine, and elevated levels of lipoperoxide. It was concluded that mortality was due to myocarditis associated with the ingestion of rancid feed.     

Organization of the ribosomal ribonucleic acid genes in various wild-type strains and wild-collected strains of Neurospora

Summary The organization of the ribosomal DNA (rDNA) repcat unit in the standard wild-type strain of Neurospora crassa, 74-OR23-1A, and in 30 other wild-type strains and wild-collected strains of N. crassa, N. tetrasperma, N. sitophila, N. intermedia, and N. discreta isolated from nature, was investigated by restriction enzyme digestion of genomic DNA, and probing of the Southern-blotted DNA fragments with specific cloned pieces of the rDNA unit from 74-OR23-1A. The size of the rDNA unit in 74-OR23-1A was shown to be 9.20 kilobase pairs (kb) from blotting data, and the average for all strains was 9.11+0.21 kb; standard error=0.038; coefficient of variation (C.V.)=2.34%. These data indicate that the rDNA repeat unit size has been highly conserved among the Neurospora strains investigated. However, while all strains have a conserved HindIII site near the 5 end of the 25 S rDNA coding sequence, a polymorphism in the number and/or position of HindIII sites in the nontranscribed spacer region was found between strains. The 74-OR23-1A strain has two HindIII sites in the spacer, while others have from 0 to at least 3. This restriction site polymorphism is strain-specific and not species-specific. It was confirmed for some strains by restriction analysis of clones containing most of the rDNA repeat unit. The current restriction map of the 74-OR23-1A rDNA repeat unit is presented.     

Prostaglandin 12 reduces activation of human arterial smooth muscle cells in-vivo

Patients suffering from peripheral vascular disease have been “ultima ratio”-treated with PGI2 at a rate of 5 ng/kg/min for 6 hours a day and 5 consecutive days i.v. 20 of them underwent surgery thereafter as therapy was not sufficient. A histological examination and quantification of vascular tissue revealed that the number of activated smooth muscle cells was significantly lower in treated patients vascular segments than in untreated ones in all the different age groups. A comparable suppression was found in the intima and the media as well. It is thus concluded, that PGI2 inhibits smooth muscle cell proliferation most probably by inhibiting PDGF-release from the platelets and stimulation of smooth muscle cell cAMP. To achieve a more beneficial PGI2-effect at the vascular level, a prolonged PGI2-therapy looks rather promising.