Binding of ciprofloxacin labelled with technetium Tc 99m versus 99mTc-pertechnetate to a live and killed equine isolate of Escherichia coli

This paper describes a simple methodology for evaluating the bacterial binding of ciprofloxacin labelled with technetium Tc 99m. Using this methodology, the binding of 99mTc-ciprofloxacin by live Escherichia coli was compared with the binding of 99mTc-ciprofloxacin by killed E. coli and the binding of 99mTc-pertechnetate (99mTcO4-) by live E. coli. The antimicrobial effect of 99mTc-ciprofloxacin on E. coli was evaluated. Four groups were defined: live E. coli with 99mTc-ciprofloxacin, live E. coli with 99mTcO4 , killed E. coli with 99mTc-ciprofloxacin, and killed E. coli with 99mTcO4-. After 0, 2, and 4 h of incubation of 1 x 10(8) colony-forming units of E. coli suspended in 5 mL of sterile distilled water with 1.85 MBq of 99mTc-ciprofloxacin or 99mTcO4, 1 mL from each sample was centrifuged. The radioactivity of the bacterial pellet and that of the supernatant were measured separately, and the percentage of sample radioactivity attributable to bacterial binding was calculated. Of the 99mTc-ciprofloxacin, 3.6% to 5.9% was bound to live or killed E. coli; only 0.1% to 0.2% of the 99mTcO4- was bound to live E. coli (P < 0.0001). No significant difference in 99mTc-ciprofloxacin binding was found between live and killed E. coli (P = 0.887). An antimicrobial effect on E. coli was seen with 99mTc-ciprofloxacin: colony counts were reduced after 4 h. The small amount of 99mTc-ciprofloxacin binding and the lack of difference in binding between live and killed E. coli may limit the utility of this methodology in evaluating the presence of E. coli infection.     

Evaluation of an air-filtration system for preventing aerosol transmission of Porcine reproductive and respiratory syndrome virus

The purpose of this study was to evaluate the ability of a commercial air-filtration system to reduce aerosol transmission of Porcine reproductive and respiratory syndrome virus (PRRSV). The system consisted of a pre-filter and 2 filters with EU8 and EU13 ratings. In each of 4 trials, 5 PRRSV-infected donor pigs and 1 naive recipient pig (each 25 kg) were housed in opposing chambers connected by a 1.3-m-long duct. The system filtered air entering 1 recipient-pig chamber (filtered facility) from the donor-pig chamber but not a 2nd recipient-pig chamber (nonfiltered facility). The donor pigs had been experimentally infected with PRRSV MN-184, an isolate previously documented to be shed at a high frequency in contagious aerosols. On days 3 to 7 after infection of the donors, the 2 groups were housed in their respective chambers for 6 h and then in separate facilities, where samples were collected for testing by polymerase chain reaction and enzyme-linked immunosorbent assay over 14 d. Aerosol transmission was observed in 6 of the 20 replicates in the nonfiltered facility, whereas all pigs remained PRRSV-negative in the filtered facility; the difference was significant at P < 0.01. Thus, under the conditions of this study, the air-filtration system evaluated appeared to be highly effective at reducing aerosol transmission of PRRSV.     

Inheritance of fenvalerate and carbofuran resistance in colorado beetles—Leptinotarsa decemlineata (Say)—from North Carolina

Progeny from reciprocal F1 crosses and F1 backcrosses between fenvalerate-resistant and fenvalerate-susceptible Colorado beetles, Leptinotarsa decemlineata (Say), and between carbofuran-resistant and carbofuran-susceptible Colorado beetles were bioassayed to investigate the mode of inheritance of resistance to these chemicals. Bioassays of progeny from these crosses indicate that resistance to fenvalerate is inherited in a semi-recessive, sex-linked manner and carbofuran resistance is inherited in a partially dominant autosomal fashion. Log concentration/probit mortality lines and chi-square tests, however, indicate that multiple genes may be involved in resistance to both insecticides.     

Measurement of acephate and its principal metabolite in leaves by gas-liquid chromatography

A semi-micro method is described for monitoring levels of acephate (O, S-dimethyl acetylphosphoramidothioate) and its principal metabolite, methamidophos (O, S-dimethyl phosphoramidothioate) in leaf material derived from treated, hydroponically grown gerberas (Gerbera jamesonii H. Bollus, ex Hook. f.) To minimise injury to the living leaf, analyses were performed on 13-mm diameter discs punched from the interveinal regions of the lamina. The leaf disc samples were then extracted with ethyl acetate. Clean-up of extracts was accomplished by passing the filtered leaf extracts through glass mini-columns containing carbon + filter aid (2 + 5 by mass). Acephate and methamidophos were eluted from the column with methanol and measured simultaneously by programmed temperature gas chromatography using a thermionic specific detector.     

黄瓜花叶病毒外壳蛋白质进入叶绿体与症状发生的关系

 由感染黄瓜花叶病毒(CMV)、健康和转外壳蛋白(CP)基因的烟叶以原生质体法制备纯化的叶绿体。经SDS-PAGE电泳,银染色,比较其蛋白质图谱。用CMV外壳蛋白游离亚基制备的抗血清进行Western blotting。结果发现:1.CP存在于CMV侵染的烟叶绿体中。2.叶绿体中CP的浓度和花叶症状严重程度呈正相关;3.表达CP的转基因烟草叶绿体中未测出CP存在。根据以上结果,认为CMV侵染的烟花叶症状产生与CP进入叶绿体有直接相关性。     

The transmission by nematodes of tobraviruses is not determined exclusively by the virus coat protein

The coat protein gene of the nematode non-transmissible, SP5 isolate of pea early-browning tobravius was replaced with that of the highly nematode transmissible, PPK20 isolate of tobacco rattle tobravirus. Plants were infected with the recombinant virus when mechanically inoculated and the virus invaded the plants systemically. However, although the PPK20 isolate of TRV was transmitted by nematodes from these plants, the recombinant virus was not transmitted. Therefore, the virus coat protein is not the exclusive determinant of nematode transmission.     

Inhibition of juvenile hormone biosynthesis and methyl farnesoate epoxidase activity by 1,5-disubstituted imidazoles in the cockroach,Diploptera punctata

Seventeen substituted imidazoles were tested as inhibitors of juvenile hormone (JH) III synthesis by cockroach corpora allata in an in-vitro radio-chemical assay. Most of these 1,5-disubstituted imidazoles were highly potent, with IC₅₀ values of less than 100nM. The compounds differed in their ability to cause an accumulation of the precursor methyl farnesoate in the glands. Four of the imidazoles were tested by topical application to previtellogenic adult females, and all caused a significant inhibition of JH synthesis and an accumulation of intraglandular methyl farnesoate for at least three days after treatment. Methyl farnesoate epoxidase activity of homogenates of corpora allata was inhibited by the compounds TH -14 and TH -27. This P450-dependent epoxidase activity was inhibited at less than 10 nM. The results show that the 1,5-disubstituted imidazoles are powerful inhibitors of the last step of juvenile synthesis in this cockroach.