Publications by authors named "Nikita Nirwan"

Background: Diabetic osteoporosis is a poorly managed serious skeletal complication, characterized by high fracture risk, increased bone resorption, reduced bone formation, and disrupted bone architecture. There is a need to investigate drugs that can improve bone health along with managing glycemic control. DPP-4 inhibitors and metformin have proven benefits in improving bone health.

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Comorbid conditions in persons with epilepsy (PWE) are very common with depression being highly prevalent. Lacosamide (LCM) is used to treat patients with seizures, but the underlying pathways associating the seizures and comorbid depression are still unknown. Kynurenine pathway (KP) has a major role in seizures, inflammation as well as depression, considering which we evaluated the effect of LCM on kynurenine levels in murine model of neuroinflammation-mediated seizures.

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: Treatment of osteoporosis with the available drug formulations is still challenging due to multiple associated limitations such as chronic treatment, off-target side effects, poor bone targeting, and low bioavailability. Adopting advanced bone-targeted drug delivery strategies like liposomes is one of the safe and effective approaches for osteoporosis treatment.: This review summarizes the applications of liposomes in gene delivery, bone regeneration, bone-targeted delivery, and as a carrier for drug encapsulation in the treatment of osteoporosis.

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Objective: Currently, lacosamide (LCM) is not approved for use in status epilepticus (SE) but several shreds of evidence are available to support its use. The present study was, therefore, undertaken to evaluate the effect of LCM on pilocarpine (PILO) induced SE and neurodegeneration in C57BL/6 mice and to ascertain the involvement of CRMP-2 in mediating above effect.

Methods: Pilocarpine-induced SE model was developed to explore the effect of LCM 20, 40 and 80 mg/kg in mice.

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Temporal lobe epilepsy (TLE) is the chronic and pharmacoresistant form of epilepsy observed in humans. The current literature is insufficient in explicating the comprehensive mechanisms underlying its pathogenesis and advancement. Consequently, the development of a suitable animal model mimicking the clinical characteristics is required.

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