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Evaluation of anthelmintic activity of any drug when carried out in laboratory conditions by using the isolated worms from nature cannot be adaptable with artificial laboratory conditions. Therefore, the present study aims at developing a new adaptable method for evaluation of anthelmintic activity. The present anthelmintic activity study reveals a new methodology with housefly worms cultured in laboratory conditions that resemble parasitic pinworms found in human being. We studied the anthelmintic activities of various drugs on housefly worms and earthworms. The results showed that the housefly worms had taken more time for paralysis and death. Even after paralysis the time taken for death is more in housefly worms in spite of smaller size and lesser weight of the worms compared to earthworms. The study concluded that the earthworms have not adapted to the artificial laboratory conditions leading to erratic results. Therefore, culturing of housefly worms was carried out to evaluate the anthelmintic activity and found an easy, prominent, eco-friendly, and reproducible method in all aspects such as equal age, size, and weight of worms used for the experiment.

Takshaka (Sanskrit: , IAST: Takaka) is a Nagaraja in Hinduism and Buddhism. He is mentioned in the Hindu epic Mahabharata. He is described to be a king of the Nagas and one of the sons of Kadru.

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Takshaka also known in Chinese and Japanese mythology as being one of the "eight Great Dragon Kings" ( Hachi-dai Ryuu-ou),[1] they are the only snakes which can fly and also mentioned as the most venomous snakes, amongst Nanda (Nagaraja), Upananda, Sagara (Shakara), Vasuki, Balavan, Anavatapta and Utpala.

Takshaka, disguised as a beggar, stole the earrings of Paushya king's queen, which she had given as a gift to a Brahmin named Uttanka. Uttanka managed to get it back with the help of others. He wished to revenge on Takshaka and proceeded towards Hastinapura, the capital of Kuru king Janamejaya, the great-grandson of Arjuna. Uttanka then waited upon King Janamejaya who had some time before returned victorious from Takshashila. Uttanka reminded the king of his father Parikshit's death, at the hands of Takshaka (1,3).

On examination, her best corrected visual acuity was 20/200 in right eye and 20/120 in left eye. Right eye showed mild conjunctival congestion and corneal haze. On slit lamp evaluation, a translucent worm of ~15 mm length was found freely moving in anterior chamber without any attachment to iris [Fig. 1]. There were no cells or flare in anterior chamber. Both pupils were reacting briskly to light. Both the eyes had nuclear sclerosis grade II. Undilated fundus examination of both eyes did not reveal any patch of chorioretinitis or any migratory tracts with optic discs being normal. Extra ocular movements were normal. There were no abnormalities in the surrounding adnexa. Systemic examination did not reveal any migratory subcutaneous swelling, nodules or abscess.

Her B-scan of both eyes was normal. The haemogram including eosinophil count, liver profile, renal profile and chest x-ray were normal. Routine stool and urine examination did not reveal any eggs/worm/larva. Thick smear for microfilaria came out to be negative.

Most of the times Raja carried the sacred casket at the annual perahera in Kandy flanked by Skanda and another tusker elephant. Sometimes Skanda too carried the casket, but Raja was the casket bearer of the important final Randoli perehera. Even after the demise of Skanda, the fellow tusker elephant in 1986, Raja continued his responsibilities as the chief tusker of the Esala procession in 1987. After serving Buddhist processions for about 50 years, Raja died in July 1988 due to an illness and his death prompted the government to order a day of national mourning in Sri Lanka. A postage stamp was issued in its memory on 12 December 1989, and also the 1,000 Rupee bill, with Raja and the Muslim trainer Umar Lebbe Panicker from Eravur in Batticola.[3]

Cisplatin kills proliferating cells via DNA damage but also has profound effects on post-mitotic cells in tumors, kidneys, and neurons. However, the effects of cisplatin on post-mitotic cells are still poorly understood. Among model systems, C. elegans adults are unique in having completely post-mitotic somatic tissues. The p38 MAPK pathway controls ROS detoxification via SKN-1/NRF and immune responses via ATF-7/ATF2. Here, we show that p38 MAPK pathway mutants are sensitive to cisplatin, but while cisplatin exposure increases ROS levels, skn-1 mutants are resistant. Cisplatin exposure leads to phosphorylation of PMK-1/MAPK and ATF-7 and the IRE-1/TRF-1 signaling module functions upstream of the p38 MAPK pathway to activate signaling. We identify the response proteins whose increased abundance depends on IRE-1/p38 MAPK activity as well as cisplatin exposure. Four of these proteins are necessary for protection from cisplatin toxicity, which is characterized by necrotic death. We conclude that the p38 MAPK pathway-driven proteins are crucial for adult cisplatin resilience.

The innate immune system in C. elegans has been extensively studied for its role in protecting worms from bacterial and fungal pathogens10,11. For this response, the p38 MAP kinase pathway is one of the three signaling pathways that have the greatest impact on resistance to pathogens12,13. In the intestine, the p38 MAP kinase pathway (NSY-1/MAPKKK, SEK-1/MAPKK, PMK-1/MAPK) acts by activating the transcription factor ATF-7 via phosphorylation in response to pathogen attack13, whereas for hypodermal pathogens this pathway acts via STA-2 to drive a largely non-overlapping set of genes14. Apart from its role in pathogen resistance, the p38 MAPK pathway and the downstream immune response genes are important in the modulation of responses to dietary restriction and aging15, repair of sterile wounds16, and the regulation of developmental sleep17. Work in Drosophila shows that the innate immune genes have roles in processes as diverse as in oogenesis18 and repair of traumatic brain injury19. This has led to the recognition that the immune response genes should be considered as stress modulators or repair factors and that their roles stretch beyond pathogen defense.

Cisplatin induces ROS in mammalian cells20 and worms9 and a substantial body of evidence supports the notion that ROS-provoked damage could lead to cell and tissue death. In worms, cisplatin leads to the oxidation of a specific chaperone-type protein ASNA-1. Oxidation of ASNA-1 perturbs the targeting of tail-anchored membrane proteins to the endoplasmic reticulum membrane9. However, it is not known whether the levels of ROS species are high enough to inflict damage on tissues at a level sufficient to cause extensive damage or death. ROS detoxification in response to ROS accumulation is driven by the activity of type II detoxification genes which are under control of the SKN-1/NRF transcription factor. Phosphorylation and activation of SKN-1 is in turn mediated upstream by the activation of p38 MAPK pathway components SEK-1 and PMK-1 in response to increased ROS levels21,22,23. It is, therefore, possible to test, using C. elegans as a model, whether ROS-induced toxicity is an important aspect of cisplatin-provoked death.

In this study, using a combination of quantitative proteomics, genetic analysis, and selective degradation of signaling molecules we find that the p38 MAP kinase pathway has an important function in ensuring survival on cisplatin. However, we find that the activation of the innate immune response genes downstream of this pathway is far more important than the ROS detoxification arm in mediating the cisplatin response. Restricting the signaling only in somatic tissues of post-mitotic adults is equivalent to a complete knockout of the pathway observed in null mutants. Cisplatin-induced ROS is important for activation of the signaling activity and the transcription factor ATF-7 acting downstream of the p38 MAPK signaling pathway is a central participant in the response. Consistent with this idea we found that PMK-1/MAPK and ATF-7 are phosphorylated upon cisplatin exposure and that ATF-7 phosphorylation requires PMK-1 function. Moreover, IRE-1 functions with TRF-1 in a UPRER-independent manner upstream of the p38 MAPK pathway to initiate signaling. We find that sulfenylation of IRE-1 is an early molecular event in response to cisplatin exposure and this molecular landmark in turn leads to the accumulation of innate immune proteins. We identify a set of immune response proteins whose abundance depends on SEK-1 and cisplatin. Strikingly, mutants in several of these innate immune response proteins are also cisplatin sensitive. The mutants accumulate phosphatidyl serine on the surface of the necrotic vacuoles and mutants defective in excretory canal function (the kidney equivalent in worms) function are also cisplatin sensitive. We conclude that in post-mitotic tissues, the IRE-1/PMK-1/ATF-7 pathway function is of greater importance than the ROS detoxification pathway to promote resilience against cytotoxicity.

There is a well-established function of ROS in the activation of MAPKs when mammalian cells are treated with cisplatin24. It was previously shown that cisplatin induces ROS in 1-day-old adult animals9. We found evidence that cisplatin treatment leads to ROS-promoted protein damage (Supplementary Fig. 1a, b). Mindful of the role of p38 MAPK activation upon ROS accumulation, we asked if the p38 MAPK cascade has functions in adult animals in response to cisplatin exposure. We found this to be the case based on several observations. First, cisplatin exposure induced the p38 MAPK pathway activity as monitored by the phosphorylation of PMK-1/MAPK (Fig. 1a, b; Supplementary Fig. 2), and cisplatin-induced ROS was required for p38 activation since treating with a ROS scavenger (MitoTempo) resulted in a decrease in PMK-1 phosphorylation (Fig. 1c, d; Supplementary Fig. 2). Second, cisplatin treatment led to an increase in the accumulation PMK-1::mNeonGreen25 in the intestinal nuclei in comparison to the untreated controls (Supplementary Fig. 3). Third, mutants in p38 MAPK pathway sek-1(km4)/MAPKK and pmk-1(km25)/MAPK, were sensitive to cisplatin in comparison to the wild-type animals (Fig. 1e). The LD50 of sek-1(km4) mutants for cisplatin-induced death was 150 g/mL (Supplementary Fig. 4), which is half the dose of well-studied cisplatin sensitive mutants in asna-18 and about 3.5 times lower than that of wild-type animals. Another sek-1 deletion mutant, syb2311, created by precise deletion of the entire coding sequence of sek-1, also showed enhanced sensitivity to cisplatin treatment, at levels comparable to those seen in sek-1(km4) mutants (Fig. 1e)25. We concluded that cisplatin treatment led to activation of the p38 MAPK pathway and that the activation was ROS dependent. ff782bc1db