What is he best known for?
The fields of study he is best known for:
- Gene
- Internal medicine
- Enzyme
Immunology, Acute pancreatitis, Pharmacology, Biochemistry and Pancreatitis are his primary areas of study.
His Immunology study which covers Lung injury that intersects with ARDS.
His studies deal with areas such as Multiple organ dysfunction syndrome and Pathology as well as Acute pancreatitis.
His Pharmacology research incorporates elements of Proinflammatory cytokine and Myeloperoxidase.
His Biochemistry study combines topics in areas such as Mediator and Vasodilation.
The Pancreatitis study combines topics in areas such as Necrosis and Pancreatic disease.
His most cited work include:
- Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome (866 citations)
- Hydrogen sulfide is a novel mediator of lipopolysaccharide-induced inflammation in the mouse (629 citations)
- Inflammatory mediators in acute pancreatitis. (454 citations)
What are the main themes of his work throughout his whole career to date?
Madhav Bhatia mainly investigates Immunology, Acute pancreatitis, Inflammation, Internal medicine and Sepsis.
He has included themes like Lung injury and Pharmacology in his Immunology study.
His Pharmacology research focuses on subjects like Nitric oxide, which are linked to Biochemistry.
His Acute pancreatitis research includes elements of Necrosis, Disease, Pathology and Acinar cell, Pancreatitis.
His Inflammation study also includes fields such as
- Mediator, which have a strong connection to Hydrogen sulfide,
- Cystathionine gamma-lyase which connect with Gene silencing and Lipopolysaccharide.
His Internal medicine study combines topics from a wide range of disciplines, such as Gastroenterology and Endocrinology.
He most often published in these fields:
- Immunology (40.78%)
- Acute pancreatitis (36.31%)
- Inflammation (36.31%)
What were the highlights of his more recent work (between 2015-2021)?
- Inflammation (36.31%)
- Immunology (40.78%)
- Acute pancreatitis (36.31%)
In recent papers he was focusing on the following fields of study:
Madhav Bhatia spends much of his time researching Inflammation, Immunology, Acute pancreatitis, Internal medicine and Sepsis.
Specifically, his work in Inflammation is concerned with the study of Myeloperoxidase.
He works in the field of Immunology, focusing on Cytokine in particular.
His Acute pancreatitis study deals with Innate immune system intersecting with Pancreatitis.
His work carried out in the field of Internal medicine brings together such families of science as Gastroenterology and Diabetes mellitus, Endocrinology.
His Sepsis research incorporates themes from Substance P, Intensive care unit, Ligation and Liver immunology.
Between 2015 and 2021, his most popular works were:
- Sulforaphane Protects Pancreatic Acinar Cell Injury by Modulating Nrf2-Mediated Oxidative Stress and NLRP3 Inflammatory Pathway. (42 citations)
- Therapeutic implications of innate immune system in acute pancreatitis. (27 citations)
- Fasting levels of insulin and amylin after acute pancreatitis are associated with pro-inflammatory cytokines. (21 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Internal medicine
- Enzyme
Madhav Bhatia focuses on Immunology, Internal medicine, Endocrinology, Inflammation and Acute pancreatitis.
His Severity of illness research extends to Immunology, which is thematically connected.
His work on Glutathione peroxidase and Inflammasome as part of his general Internal medicine study is frequently connected to Resistin, Adipokine and Ceruletide, thereby bridging the divide between different branches of science.
His research integrates issues of Cystathionine gamma-lyase, Rheumatoid arthritis, Lung and Sepsis in his study of Inflammation.
The study incorporates disciplines such as Cytokine, Pharmacology, Gene silencing, Mediator and Myeloperoxidase in addition to Cystathionine gamma-lyase.
His Acute pancreatitis study incorporates themes from Innate immune system, Clinical trial, Disease and Pancreatitis.
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