Two different Spodoptera littoralis (Boisd.) (Lepidoptera: Noctuidae) nucleopolyhedrovirus (SpliNPV) isolates were obtained from natural infected S. littoralis larvae in Egypt. The phylogenetic analysis of the partial nucleotide sequence of the polyhedrin gene (polh) showed that both isolates, Spli-6 and Spli-7, were closed and had a common ancestor with S. littoralis NPV isolate 1263 polyhedrin gene, partial coding sequence with accession number AGE90003.1 that belongs to group II NPVs. This indicates that the natural host of Spli-6 and Spli-7 must be S. littoralis. The virulence of these isolates was tested against S. littoralis larvae in a laboratory. The LC 50 against 1st instar larvae was significantly different, 3 × 10 4 OBs/ml and 9.5 × 10 4 OBs/ml for Spli-6 and Spli-7, respectively. However, the LC 50 for the mixed infection of both isolates was 3.9 × 10 4 OBs/ml. On the other hand, the ST 50 was 96 h for both isolates, while it was 120 h for the mixed infection, which was higher than that observed of each single isolate. Upon digestion of viral DNA with ScaI endonuclease, the restriction profile showed one more fragment of about~25 kbp and 3 fragments of about~19,~5.8, and~5.3 kbp in Spli-7 isolate compared to Spli-6 as well as the reference strain SpliNPV-AN1956. The differences in the fragment size and number suggest the existence of genotypic variants between both isolates. Spli-6 and Spli-7 proved to possess promising insecticidal properties for the development of virus-based biopesticide for the control of S. littoralis.

Propafenone is a well‐known Class 1C antiarrhythmic agent that has sodium channel blocking properties as well as the ability to block 13 other channels and a modest calcium antagonistic effect. Propafenone has a profound electrophysiologic effect on auxiliary atrioventricular circuits and in patients with atrioventricular nodal reentry tachycardia can obstruct conduction in the fast conducting pathway. Furthermore, propafenone is less likely than other Class 1C drugs to cause proarrhythmia. However, although this medicine can pass through the placenta, the effects during pregnancy remain unknown. Here, we investigated the potential teratogenic and genotoxic effects of Rythmol during rat development. Pregnant Wistar rats received 46.25 mg/kg body weight of propafenone daily by gavage from Gestation Day (GD) 5 to GD 19. At GD 20, the dams were dissected, and their fetuses were assessed via morphologic, skeletal, and histologic investigation. In addition, a comet assay was used to measure DNA impairment of fetal skull osteocytes and hepatic cells. The study showed that propafenone treatment of pregnant rats led to a marked decrease in gravid uterine weight, number of implants/litter, number of viable fetuses, and bodyweight of fetuses but a clear increase in placental weight and placental index in the treated group. Frequent morphologic abnormalities and severe ossification deficiency in the cranium bones were observed in the treatment group. Various histopathological changes were observed in the liver, kidney, and brain tissues of maternally treated fetuses. Similarly, propafenone induced DNA damage to examined samples. Thus, our study indicates that propafenone may be embryotoxic in humans.