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In the present study, the ethanolic root extract of Desmodium gangeticum (L.) DC., Fabaceae, (EDG), have been studied in various acute and chronic ulcer mouse models. Oral administration of root extract, significantly decrease the ulcer index and lesion number in a dose dependent manner against ethanol induced acute gastric ulcer in mice. In gastric ulcerated animal that received high dose of 150 mg/kg EDG, the mucosa showed no ulceration with slight focal congestion and the glands appeared normal. Pylorus ligated mice, pretreated with EDG showed significant decrease in ulcerous activity under chronic condition. The highest dose (150 mg/kg) of the extract provoked a marked increase in protein and glutathione levels, when compare to control. Furthermore, gastric juice, free acidity and total acid output were inhibited in a dose-dependent manner at p<0.05 level. Our results indicate that the EDG possess gastroprotective activity and increasing regeneration of damaged gastric mucosa and thus safe for human use.

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Alzheimer's disease (AD) is a devastative neurodegenerative disorder which needs adequate studies on effective treatment options. The extracts of plants and their effect on the amelioration of AD symptoms have been extensively studied. This paper summarizes the mechanisms like acetylcholinesterase (AChE) inhibition, modification of monoamines, antiamyloid aggregation effect, and antioxidant activity which are actively entailed in the process of amelioration of AD symptoms. These effects are induced by extracts of a few plants of different origin like Yizhi Jiannao, Moringa oleifera (Drumstick tree), Ginkgo Biloba (Ginkgo/Maidenhair tree), Cassia obtisufolia (Sicklepod), Desmodium gangeticum (Sal Leaved Desmodium), Melissa officinalis (Lemon Balm), and Salvia officinalis (Garden sage, common sage).

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Alzheimer's disease is a neurodegenerative disorder with unclear etiology for a few decades. Many animal models employed to study the etiology of the disease and test the efficacy of a drug could give limited understanding of these events. Introduction of aluminum salts into aged New Zealand rabbit brain could demonstrate neurofibrillary tangle formation in 1965. This outstanding contribution substantiated the role of aluminum in Alzheimer's disease in turn becoming the basis further molecular studies in rabbits. In this review, various animal models (transgenic mice, rats, rabbits, zebrafish) used to study the pathology of the disease and to test the efficacy of a drug have been summarized. It also focuses on the growing need to unravel the molecular underpinnings of the disease progression.

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Deoxyribonucleic acid (DNA) damage has been implicated in ageing and neurodegenerative disorders including Alzheimer's disease (AD) for a few decades. Although it is an established finding, yet there are limited studies on DNA damage. In both nucleus and mitochondria, DNA damage is primarily free radical mediated. It has been proven that mitochondrial DNA is more vulnerable to damage compared to the nuclear DNA. A few studies summarized in this review throw light on the mechanisms of free radical mediated DNA damage and impairment of DNA repair mechanisms in AD. There is a growing need to initiate studies on DNA damage and repair and unravel the molecular underpinnings entailed in the etiopathogenesis of the disease. The outcome of such studies substantiates the corner stone streamlined to employ therapeutic strategies.

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BACKGROUND: Alzheimers disease (AD) is a devastative neurodegenerative disorder. Lack of substantial animal model that can unravel molecular underpinnings has been a major lacuna which limited the understanding of the etiology of the disease in turn limiting the employment of potential therapeutic strategies to combat the disease for a few decades. Our studies for the first time provided substantial animal model and tattered the etiology of the disease at a molecular level. METHODS: In this study DNA was isolated from Hippocampus (H), Midbrain (M) and Frontal Cortex (Fc) of control and aluminium maltolate (Al-M) treated aged New Zealand rabbit brain. DNA damage has been studied using Agarose gel electrophoresis, Ethidium Bromide (EtBr) binding and Melting temperature techniques. RESULTS: Al-M treated aged New Zealand rabbit's H and M showed higher DNA damage compared to corresponding controls, where as Fc showed mild DNA damage compared to corresponding controls. CONCLUSIONS: This study tangibly provides substantial molecular level understanding of the disease in turn providing an adequate platform to streamline potential therapeutic strategies. KEYWORDS: Alzheimer's disease; Aluminium maltolate; Animal model; DNA damage.

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Lysyl tRNA synthetases facilitate amino acylation and play a crucial role in the essential cellular process of translation. They are grouped into two distinct classes (class I and class II). Class I lysyl tRNA synthetase is considered as a drug target for syphilis caused by Treponema pallidum. Comparative genome analysis shows the absence of its sequence homolog in eukaryotes. The structure of class I lysyl tRNA synthetase from Treponema pallidum is unknown and the difficulties in the in vitro culturing of Treponema makes it non-trivial. We used the structural template of class I lysyl tRNA synthetase from the archaea Pyrococcus horikoshii for modeling the Treponema pallidum lysyl tRNA synthetase structure. Thus, we propose the usefulness of the modeled class I lysyl tRNA synthetase for the design of suitable inhibitors towards the treatment of syphilis.