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Vijay V. Kakkar

Bio: Vijay V. Kakkar is an academic researcher from University of Cambridge. The author has contributed to research in topics: Heparin & Thrombosis. The author has an hindex of 60, co-authored 470 publications receiving 17731 citations. Previous affiliations of Vijay V. Kakkar include University of Oslo & National Institute for Biological Standards and Control.


Papers
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Journal ArticleDOI
TL;DR: 132 consecutive patients were investigated during the postoperative period using the 125 I-labelled fibrinogen test to detect deep-vein thrombosis in the legs to indicate which patients are at risk and which require active treatment.

830 citations

Journal ArticleDOI
TL;DR: Impaired myocardial angiogenesis and ischemic cardiomyopathy in mice lacking the vascular endothelial growth factor isoforms V EGF 164 and VEGF 188 is observed.
Abstract: Impaired myocardial angiogenesis and ischemic cardiomyopathy in mice lacking the vascular endothelial growth factor isoforms VEGF 164 and VEGF 188

697 citations

Journal ArticleDOI
TL;DR: Two hundred and three patients undergoing elective surgery were investigated to determine the group of patients who are at a “great risk” of developing deep vein thrombosis during the postoperative period, and it was found that the patients who formed this group included those who had a history of previous deep vein dilation or pulmonary embolism.
Abstract: Summary Two hundred and three patients undergoing elective surgery were investigated to determine the group of patients who are at a “great risk” of developing deep vein thrombosis. It was found that the patients who formed this group included those who had a history of previous deep vein thrombosis or pulmonary embolism, those who had varicose veins or underwent operation for malignant disease, and elderly patients (over sixty-one years) having major operations. All of these patients are at a “great risk” of developing thrombosis during the postoperative period.

418 citations


Cited by
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Journal ArticleDOI
TL;DR: Vascular endothelial growth factor (VEGF) is a key regulator of physiological angiogenesis during embryogenesis, skeletal growth and reproductive functions and is implicated in pathologicalAngiogenesis associated with tumors, intraocular neovascular disorders and other conditions.
Abstract: Vascular endothelial growth factor (VEGF) is a key regulator of physiological angiogenesis during embryogenesis, skeletal growth and reproductive functions. VEGF has also been implicated in pathological angiogenesis associated with tumors, intraocular neovascular disorders and other conditions. The biological effects of VEGF are mediated by two receptor tyrosine kinases (RTKs), VEGFR-1 and VEGFR-2, which differ considerably in signaling properties. Non-signaling co-receptors also modulate VEGF RTK signaling. Currently, several VEGF inhibitors are undergoing clinical testing in several malignancies. VEGF inhibition is also being tested as a strategy for the prevention of angiogenesis, vascular leakage and visual loss in age-related macular degeneration.

8,942 citations

Journal ArticleDOI
14 Sep 2000-Nature
TL;DR: Pathological angiogenesis is a hallmark of cancer and various ischaemic and inflammatory diseases and integrated understanding is leading to the development of a number of exciting and bold approaches to treat cancer and other diseases, but owing to several unanswered questions, caution is needed.
Abstract: Pathological angiogenesis is a hallmark of cancer and various ischaemic and inflammatory diseases Concentrated efforts in this area of research are leading to the discovery of a growing number of pro- and anti-angiogenic molecules, some of which are already in clinical trials The complex interactions among these molecules and how they affect vascular structure and function in different environments are now beginning to be elucidated This integrated understanding is leading to the development of a number of exciting and bold approaches to treat cancer and other diseases But owing to several unanswered questions, caution is needed

8,561 citations

Journal ArticleDOI
01 Oct 1992-Chest
TL;DR: The risk factors for VTE among hospitalized patients are outlined, the efficacy and safety of alternative prophylaxis regimens are reviewed, and recommendations regarding the most suitable prophymic regimens based on the estimated risk are provided.

4,360 citations

Journal ArticleDOI
TL;DR: The cellular and molecular mechanisms underlying the formation of endothelium-lined channels and their maturation via recruitment of smooth muscle cells (arteriogenesis) during physiological and pathological conditions are summarized, alongside with possible therapeutic applications.
Abstract: Endothelial and smooth muscle cells interact with each other to form new blood vessels. In this review, the cellular and molecular mechanisms underlying the formation of endothelium-lined channels (angiogenesis) and their maturation via recruitment of smooth muscle cells (arteriogenesis) during physiological and pathological conditions are summarized, alongside with possible therapeutic applications.

4,154 citations