Author
Yashdeep Gupta
Other affiliations: M.G.M. Medical College, Mahatma Gandhi Memorial Medical College, Government Medical College, Thiruvananthapuram ...read more
Bio: Yashdeep Gupta is an academic researcher from All India Institute of Medical Sciences. The author has contributed to research in topics: Gestational diabetes & Diabetes mellitus. The author has an hindex of 23, co-authored 201 publications receiving 1896 citations. Previous affiliations of Yashdeep Gupta include M.G.M. Medical College & Mahatma Gandhi Memorial Medical College.
Papers published on a yearly basis
Papers
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TL;DR: The findings suggest that ginger could be an effective and cheap antiemetic adjunct to cancer chemotherapy and neither of the ginger extract was effective against apomorphine-induced emesis.
127 citations
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TL;DR: The pathophysiology behind glucocorticoid-induced myopathy, along with diagnostic features and treatment, are discussed, and patients with Cushing's syndrome are referred for treatment.
Abstract: Glucocorticoid-induced myopathy is the most common type of drug-induced myopathy Nearly 60% of patients with Cushing's syndrome have muscle weakness Glucocorticoid-induced muscle atrophy affects mainly fast-twitch glycolytic muscle fibers (type IIb fibers) This brief review will discuss the pathophysiology behind glucocorticoid-induced myopathy, along with diagnostic features and treatment
126 citations
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TL;DR: The antiemetic effect of the acetone and ethanolic extract of ginger (Zingiber officinale, Roscoe, Zingiberacae) against cisplatin-induced emesis in dogs was demonstrated and ginger juice produced better reversal than ondansetron.
119 citations
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TL;DR: Oral treatment of animals with 400 mg/kg body weight of Withania somnifera extract significantly reduced the tumour incidence, tumour volume and enhanced the survival of the mice, compared with 20‐methylcholanthrene injected mice, which may be due to its antioxidant and detoxifying properties.
Abstract: The current experimental work deals with the chemopreventive studies of a hydroalcoholic extract of Withania somnifera roots, against 20-methylcholanthrene induced fibrosarcoma tumours in Swiss albino mice. A single subcutaneous injection of 200 microg 20-methylcholanthrene in 0.1 mL of dimethylsulphoxide into the thigh region of mice produced a high incidence (96%) of tumours. Oral treatment of animals with 400 mg/kg body weight of Withania somnifera extract (one week before injecting 20-methylcholanthrene and continued until 15 weeks thereafter) significantly reduced the tumour incidence, tumour volume and enhanced the survival of the mice, compared with 20-methylcholanthrene injected mice. The tumour incidence was also delayed in the treatment group when compared with 20-methylcholanthrene injected mice. Liver biochemical parameters revealed a significant modulation of reduced glutathione, lipid peroxides, glutathione-S-transferase, catalase and superoxide dismutase in extract treated mice compared with 20-methylcholanthrene injected mice. The mechanism of chemopreventive activity of Withania somnifera extract may be due to its antioxidant and detoxifying properties.
101 citations
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TL;DR: Adiposity, increased insulin resistance, high leptin, evidence of deranged autoimmunity, all of which are present in both disease states, seem to play a complex role in connecting these two disorders.
Abstract: As the prevalence of these endocrine dysfunctions increases, the association of polycystic ovary syndrome (PCOS) and autoimmune thyroid disease is increasingly being recognised. While the causality of this association is still uncertain, the two conditions share a bidirectional relationship. The exact nature of this link has not been elucidated yet. Both syndromes share certain common characteristics, risk factors, and pathophysiological abnormalities. Simultaneously, certain etiopathogenetic factors that operate to create these dysfunctions are dissimilar. Polycystic appearing ovaries are a clinical feature of hypothyroidism, though hypothyroidism should be excluded before diagnosing PCOS. Adiposity, increased insulin resistance, high leptin, evidence of deranged autoimmunity, all of which are present in both disease states, seem to play a complex role in connecting these two disorders. This brief communication explores the nature of the relationship between PCOS and hypothyroidism. It reviews current data and analyses them to present a unified pathophysiological basis, incorporating these complex relationships, for the same.
81 citations
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01 Jan 2014
TL;DR: These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care.
Abstract: XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.
9,618 citations
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TL;DR: A diagnosis of gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that is not clearly overt diabetes) or chemical-induced diabetes (such as in the treatment of HIV/AIDS or after organ transplantation)
Abstract: 1. Type 1 diabetes (due to b-cell destruction, usually leading to absolute insulin deficiency) 2. Type 2 diabetes (due to a progressive insulin secretory defect on the background of insulin resistance) 3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that is not clearly overt diabetes) 4. Specific types of diabetes due to other causes, e.g., monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset diabetes of the young [MODY]), diseases of the exocrine pancreas (such as cystic fibrosis), and drugor chemical-induced diabetes (such as in the treatment of HIV/AIDS or after organ transplantation)
2,339 citations
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1,896 citations
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TL;DR: Physiologically, metformin has been shown to reduce hepatic glucose production, yet not all of its effects can be explained by this mechanism and there is increasing evidence of a key role for the gut.
Abstract: Metformin is a widely-used drug that results in clear benefits in relation to glucose metabolism and diabetes-related complications. The mechanisms underlying these benefits are complex and still not fully understood. Physiologically, metformin has been shown to reduce hepatic glucose production, yet not all of its effects can be explained by this mechanism and there is increasing evidence of a key role for the gut. At the molecular level the findings vary depending on the doses of metformin used and duration of treatment, with clear differences between acute and chronic administration. Metformin has been shown to act via both AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms; by inhibition of mitochondrial respiration but also perhaps by inhibition of mitochondrial glycerophosphate dehydrogenase, and a mechanism involving the lysosome. In the last 10 years, we have moved from a simple picture, that metformin improves glycaemia by acting on the liver via AMPK activation, to a much more complex picture reflecting its multiple modes of action. More work is required to truly understand how this drug works in its target population: individuals with type 2 diabetes.
1,302 citations