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Mohammad F. Kiani

Researcher at Temple University

Publications -  114
Citations -  3753

Mohammad F. Kiani is an academic researcher from Temple University. The author has contributed to research in topics: Cell adhesion molecule & Endothelium. The author has an hindex of 33, co-authored 111 publications receiving 3356 citations. Previous affiliations of Mohammad F. Kiani include Islamic Azad University & University of Rochester.

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Journal ArticleDOI

Infarct scar as living tissue.

Yao Sun, +3 more
- 01 Sep 2002 - 
TL;DR: These various components of the infarct scar that provide for its dynamic nature and which is relevant to today's interest in preventing heart failure through a rebuilding (regrowing) of myocardial tissue at theinfarct size are reviewed.
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Classification, Treatment Strategy, and Associated Drug Resistance in Breast Cancer

Yuan Tang, +4 more
- 01 Oct 2016 - 
TL;DR: It is believed that the understanding of the molecular mechanisms of each treatment and subsequent drug resistance development will eventually lead to the discovery of more effective and efficient second-line therapeutics.
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Radiation-induced permeability and leukocyte adhesion in the rat blood–brain barrier: modulation with anti-ICAM-1 antibodies

Hong Yuan, +6 more
- 18 Apr 2003 - 
TL;DR: Findings provide a target to reduce radiation-related permeability and cell adhesion and potentially the side effects of radiation in the CNS.
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Effects of fractionated radiation on the brain vasculature in a murine model: blood-brain barrier permeability, astrocyte proliferation, and ultrastructural changes.

Hong Yuan, +7 more
- 01 Nov 2006 - 
TL;DR: The cellular and microvasculature response of the brain to FRT is mediated through astrogliosis and ultrastructural changes, accompanied by an increase in BBB permeability.
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Leukocyte-inspired biodegradable particles that selectively and avidly adhere to inflamed endothelium in vitro and in vivo

Harshad S. Sakhalkar, +9 more
- 23 Dec 2003 - 
TL;DR: The leukocyte–inspired particles have adhesion efficiencies similar to that of leukocytes and were shown to target each of the major inducible endothelial cell adhesion molecules that are up-regulated at sites of pathological inflammation.