Institution
Central Drug Research Institute
Facility•Lucknow, Uttar Pradesh, India•
About: Central Drug Research Institute is a facility organization based out in Lucknow, Uttar Pradesh, India. It is known for research contribution in the topics: Catalysis & Leishmania donovani. The organization has 4357 authors who have published 7257 publications receiving 143871 citations. The organization is also known as: Central Drug Research Institute, Lucknow & CDRI.
Topics: Catalysis, Leishmania donovani, Ring (chemistry), Aryl, Apoptosis
Papers published on a yearly basis
Papers
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TL;DR: Novel fluconazole/bile acid conjugates were designed and their regioselective synthesis was achieved in very high yield via Cu(I) catalyzed intermolecular 1,3-dipolar cycloaddition and showed good antifungal activity against Candida species.
92 citations
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TL;DR: The medicinal chemistry and pharmacological properties of the multi-target molecules published since 1998 are reviewed to allow the readers to easily follow the evolution of this prominent medicinal chemistry approach to develop a more efficient inhibitor.
92 citations
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TL;DR: In this paper, B. diffusa hexane, chloroform and ethanol extracts, and two pure compounds Bd-I (eupalitin-3-O-beta-D-galactopyranoside) and Bd -II (Eupalithin) were evaluated in vitro for their effect on T cell mitogen (phytohemagglutinin; PHA) stimulated proliferation of human peripheral blood mononuclear cell (PBMC), mixed lymphocyte culture, lipopolysaccharide (LPS) stimulated nit
91 citations
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TL;DR: The increased incidence of fungal infections in the recent past has been attributed to the increase in the number of human immunodeficiency virus‐positive and AIDS patients, and early diagnosis of mycoses in patients is crucial for prompt antifungal therapy.
Abstract: The increased incidence of fungal infections in the recent past has been attributed to the increase in the number of human immunodeficiency virus-positive and AIDS patients. Early diagnosis of mycoses in patients is crucial for prompt antifungal therapy. The yield of clinical examination in the diagnosis of keratomycosis is 63-83% and KOH mount is 91%. This still highlights the limitation of routine clinical examination and smear examination, which is not performing 100% efficiently. It is for these 37%, 17% and 9% of cases, every day advanced technologies are called for. Those who deal with patient care are aware of certainties and uncertainties of results of clinical examination. The best reported figures at specialized centres might not translate into clinical practice. Another factor to be kept in mind is that many patients who come after secondary and tertiary referrals are already treated with antibiotics, antivirals, steroids and sometimes even antifungals that distort the clinical picture completely. Further, one has to consider as well the cases caused by yeast-like fungi, which resemble bacterial keratitis. Confirmation of diagnosis, not only in case of mycotic keratitis but also for other diseases, to initiate prompt and accurate therapy would avoid unnecessary and indiscriminate use of steroids/antibacterials/antivirals and antifungals.
91 citations
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TL;DR: Streptozotocin (STZ) produces similar characteristic pathology of sAD such as altered glucose metabolism, insulin signaling, synaptic dysfunction, protein kinases such as protein kinase B/C, glycogen synthase-3β activation, tau hyperphosphorylation, Aβ deposition, and neuronal apoptosis, which can be used to explore the underlying molecular and pathophysiological mechanism of AD and their therapeutic intervention for drug development against AD pathology.
Abstract: Alzheimer's disease (AD) is a neurodegenerative disorder that is remarkably characterized by pathological hallmarks which include amyloid plaques, neurofibrillary tangles, neuronal loss, and progressive cognitive loss. Several well-known genetic mutations which are being used for the development of a transgenic model of AD lead to an early onset familial AD (fAD)-like condition. However, these settings are only reasons for a small percentage of the total AD cases. The large majorities of AD cases are considered as a sporadic in origin and are less influenced by a single mutation of a gene. The etiology of sporadic Alzheimer's disease (sAD) remains unclear, but numerous risk factors have been identified that increase the chance of developing AD. Among these risk factors are insulin desensitization/resistance state, oxidative stress, neuroinflammation, synapse dysfunction, tau hyperphosphorylation, and deposition of Aβ in the brain. Subsequently, these risk factors lead to development of sAD. However, the underlying molecular mechanism is not so clear. Streptozotocin (STZ) produces similar characteristic pathology of sAD such as altered glucose metabolism, insulin signaling, synaptic dysfunction, protein kinases such as protein kinase B/C, glycogen synthase-3β (GSK-3β) activation, tau hyperphosphorylation, Aβ deposition, and neuronal apoptosis. Further, STZ also leads to inhibition of Akt/PKB, insulin receptor (IR) signaling molecule, and insulin resistance in brain. These alterations mediated by STZ can be used to explore the underlying molecular and pathophysiological mechanism of AD (especially sAD) and their therapeutic intervention for drug development against AD pathology.
91 citations
Authors
Showing all 4385 results
Name | H-index | Papers | Citations |
---|---|---|---|
Sanjay Kumar | 120 | 2052 | 82620 |
John A. Katzenellenbogen | 95 | 691 | 36132 |
Brajesh K. Singh | 83 | 401 | 24101 |
Gaurav Sharma | 82 | 1244 | 31482 |
Sudhir Kumar | 82 | 524 | 216349 |
Pramod K. Srivastava | 79 | 390 | 27330 |
Mohan K. Raizada | 75 | 473 | 21452 |
Syed F. Ali | 71 | 446 | 18669 |
Ravi Shankar | 66 | 672 | 19326 |
Ramesh Chandra | 66 | 620 | 16293 |
Manoj Kumar | 65 | 408 | 16838 |
Manish Kumar | 61 | 1425 | 21762 |
Anil Kumar Saxena | 58 | 310 | 10107 |
Sanjay Krishna | 56 | 624 | 13731 |
Naibedya Chattopadhyay | 56 | 242 | 9795 |