Background
Currently, no vaccines or modern drugs are available for dengue and chikungunya and only symptomatic relief is provided to the patients. Siddha medicine, a traditional form of indigenous medical system uses specific polyherbal formulations for the treatment of such infections with considerable success. One such polyherbal formulation for the treatment of chikungunya and dengue is
Nilavembu kudineer
(NVK). The mechanistic details of this drug as an antiviral for chikungunya virus (CHIKV) and dengue virus (DENV) is poorly understood.
Objectives
The current study was undertaken to study the efficacy of NVK as an antiviral formulation against CHIKV and DENV.
Materials and methods
Cytotoxicity assays (MTT) were performed to determine the role of NVK as an antiviral during chikungunya and dengue infections in the following conditions-i). post infection, ii). during active infections and iii) protective, not allowing virus infection.
Results
It was observed that NVK provides protection against CHIKV and DENV-2 during active infection as well can help to prevent virus infection in the cells and it mainly depends on the cellular availability of drugs for maximum protection against both the infections.
Conclusion
Our study establishes that extraction protocols are important to ensure maximum efficacy of NVK along with the time of addition of the drug during CHIKV and DENV infections in the cells. This study provides insights to the possible mode of action of NVK in
in vitro
condition during CHIKV and DENV infection.
Pũrṇa Cantirotaya Centũram (PCC), a herbometallic formulation of Siddha medicine, consists of mercury, sulphur, and gold, processed with red cotton flower and plantain stem pith juices. To evaluate its safety, acute and 28-day repeated oral toxicity studies were performed following OECD test guidelines 423 and 407, respectively. In acute study, PCC was administered orally at 5, 50, 300, and 2000 mg/kg body weight. Animals were observed for toxic signs for 14 days. Gross pathology was performed at the end of the study. In repeated dose toxicity study, PCC was administered at 2.5, 25, and 50 mg/kg body weight daily for 28 days. Satellite groups (control and high dose) were also maintained to determine the delayed onset toxicity of PCC. In acute toxicity study, no treatment related death or toxic signs were observed. It revealed that the LD50 cut-off value of PCC is between 2000 and 5000 mg/kg body weight. The repeated dose study did not show evidence of any treatment related changes in all observations up to the high dose level, when compared with the control. Histopathological examination revealed no abnormalities except mild hyperplasia of stomach in high dose group. This study provides scientific validation for the safety of PCC.
Syncytial (syn) mutants of herpes simplex virus cause cell fusion. Many syn mutations map to the synl locus, which has been identified with the gK (UL53) gene. In this work, the gK genes of eight syn mutants derived from the KOS strain were sequenced to identify residues and, possibly, domains important for the fusion activity of mutant gK. DNA sequencing showed that six mutants (syn3O, syn3l, syn32, synlO2, synlO3, and synlO5) had single missense mutations in the gK gene. Two of these, syn3l and syn32, had identical mutations that caused the introduction of a potential site for N-linked glycosylation. syn3l gK was analyzed by in vitro translation and found to utilize the novel glycosylation site. Two other mutants, syn8 and syn33, had three mutations each, resulting in three amino acid substitutions in syn8 and two substitutions in syn33. Of the 10 gK syn mutant sequences known, 8 have mutations in the N-terminal domain of gK, suggesting that this domain, which
The mncentrations of the solutes in the standard mx dosimeter were changed in order to reduce the rate of Ihermal oxidation of fermus ions in the solution. ?he modified solution contained lo-' mol dm-3 ferrous ions, lo-' mol dmw3 knzoic acid and 5 x mol d r c 3 xylenol orange in 0.04 mol dm-3 aqueous aerated sulphuric acid. The rates of thermal axidation of fermus ions do not differ significantly when the solution is stored either in glass or polypropylene mntainem. The error due U) the post-imdiation delay in dose estimation depends on the dose and a dose of about 5 Gy is most suitable. When Ihe solution is stored up to about one month More irradiation and about one month after irradiation, the error in dose estimation is less than f2%. The blank and the irradiated solutions should be stored in similar containem 0031-9155/92/112095+OBE07.50 @ 1992 IO€' Publishing U d
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