Student Research Projects

UCSD Bioengineering students work on solutions to many fundamental problems in Medicine and Biology. In the following you can find examples presented in form of questions. The answers are given in the publications referenced after the question.

Mechanotransduction by Fluid Shear in Circulating Leukocytes

Question: What is the molecular mechanism for mechanosensing in leukocytes? Answer: See Makino et al., 2006.

Q. What is the mechanism for failure of mechanotransduction in hypertension and the metabolic disease? A. Chen et al., 2010.

Q. What is the fluid stress distribution on the membrane of a leukocyte actively migrating on substrate? A. Su et al. 1997, 1998

Q. To what degree do integrins control mechanotransduction of leukocytes by fluid shear stress? A. Marschel et al., 2002

Q. Why does centrifugation of leukocytes annihilate the mechanotransduction in circualting leukocytes ? A. Fukuda et al., 2002

Microvascular Biorheology

Question: What is the mechanism by which a small number of circulating leukocytes (less than 1% by volume) imposes a large reduction of blood flow in the microcirculation even without adhering to the endothelium? Answer: see Sutton et al., 1992; Helmke et al. 1997, 1998

Q. Activated cells in the microcirculation, like leukocytes, may cause complications and don't have the ability to freely circulate. What could be a mechanism by which leukocytes become deactivated ("downregulated") in the circulation even though the cells have to be upregulated in order to migrate from the bone marrow (where they are produced) across the endothelium into the circulation? A. Moazzam et al., 1997

Q. What is a mechanosensor on a leukocyte projecting pseudpod? A. Makino et al., 2006

The Lymphatics: Unidirectional Transport for Fluids, Tissue Fragments and Immune Cells with Two Valve-systems.

Q. Lymphatics have one valve system, the classical intralymphatic bileaflet valves. Where is the second valve systems so they can transport fluid in a unidirectional way during lymph pumping? A. Trzewik et al., 2001

Q. What are the consequences when the primary valves fail? A. Lynch et al. 2007; Schmid-Schönbein, 2003

Physiological Shock: A Condition with High Mortality

Question: Which organs are the source of the powerful inflammatory cell activators that are detected already in shock? Note: the answer to this question is of extraordinary importance for understanding the mechanism for Autodigestion in shock and cardiovascular diseases. Answer: Kistler et al. 2000; Kistler et al., 2000; Waldo et al., 2003

Q. Is there a way you may be able to block the lethal progression of physiological shock ? If that were the case, physicians would have the tools to avoid many deaths in their patients. A. Mitsuoka et al., 2000, 2002; DeLano et al., 2013

Q. What is the cause of death in endotoxic shock? (It is not endotoxin! The problem is much more interesting). A. Fitzal et al., 2003

Arterial Hypertension and Diabetes: Proteolytic Receptor Cleavage

Question: A mechanism for insulin resistance (i.e. the inability to transport glucose inside a cell) in diabetes. Answer: DeLano et al., 2008; 2010

Q. What could be a mechanism by which distinct complications, e.g. hypertension, diabetes, capillary rarefaction, immune suppression, present in the same individual at the same time (e.g. as see in the metabolic syndrome X)? A. Rodrigues et al., 2010; DeLano et al., 2008; Tran et al., 2010; Chen et al., 2010; Tong et al., 2011

Q. What is the mechanism for rarefaction by which capillaries are destroyed in the microcirculation of hypertensives? A. Vogt et al., 2001; Tran et al., 2007

Q. What may be a mechanism by which hypertensives become immune-suppressed? A. Suzuki et al., 1999; Suematsu et al., 1995; DeLano et al., 2008; Chen et al., 2012; Tong et al., 2011

Q. Design a next generation sensitive technique to measure protease activity (as compared to protease protein or transcript levels) in whole blood. A. Lefkowitz et al., 2010, 2010, 2010.

Q. What is a mechanism for elevation of the unchecked protease activity in genetic hypertension? A. Wu et al., 2011

Is Oxygen Free Radical Formation a Mechanisms for Hypertension?

Q. Can you design a technology to measure oxgyen free radical production in blood of hypertensive patients? A. Lacy et al., 1998; Lacy et al., 1998

Q. How can we block the excessive oxygen free radical production in hypertensive patients ? The answer to this question is of importance to companies that are trying to develop medications for better treatment of hypertensive patients. A. Suzuki et al., 1998; Swei et al., 1999; Kobayashi et al., 2006