J.S. Martin

Purdue University, West Lafayette, IN, United States

Are you J.S. Martin?

Claim your profile

Publications (2)0 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Kidney damage and/or failure caused by urinary obstruction affects thousands of patients each year. It has been hypothesized that hypoxia and/or elevated levels of hydrostatic pressure within the kidney during obstruction contribute to renal failure. However, little research has been performed to verify this claim. Investigators have examined the effects of a single stimuli, hypoxia or elevated pressure, on renal cells and have observed functional changes, including cytoskeletal rearrangement However, during obstruction in vivo, these insults are not likely to be present in isolation. In fact, it may be the synergistic effect of these combined stimuli that leads to renal failure. Therefore, an optically compatible chamber has been designed and constructed to monitor and quantify in vitro cellular changes resulting from the combined stimuli. Real-time renal cell response can be recorded using this novel chamber, an inverted fluorescent microscope, and a computer. Ultimately, an understanding of how hypoxia and/or elevated pressure induce functional changes at the cellular level may provide insight into disease pathologies and lead to the development of novel drug and prevention therapies for renal failure.
    Bioengineering Conference, 2004. Proceedings of the IEEE 30th Annual Northeast; 05/2004
  • [Show abstract] [Hide abstract]
    ABSTRACT: Several kidney pathologies result in elevated pressures within the renal interstitial fluid, thereby affecting cell function. Traditionally, these and related studies have been performed on rigid substrates. The objective of the current study was, therefore, to better simulate in vivo conditions by performing cell studies on a variety of substrates including fibronectin, gelatin, tissue culture plasticware, glass, and PLGA. In vitro studies on these substrates were performed with tubular and medullary renal cells. Specifically, changes in cell number and microfilament arrangement were examined following exposure to pathological (180 and 300 cmH<sub>2</sub>O) pressures for 24 hours. Cell number studies provided evidence that exposure to pressures of 180 and 300 cmH<sub>2</sub>O resulted in increased tubular renal cell numbers. In contrast, pressure-exposed medullary cell numbers were decreased in response to 180 and 300 cmH<sub>2</sub>O. In both cell lines this response was more drastic in response to 300 cmH<sub>2</sub>O pressure. In addition, substrate-dependent changes in microfilament structures took place in pressure-exposed renal cells. In combination, these results prove that the function of renal cells was affected by both substrate and pressure exposure. Hopefully, elucidating such renal cell responses to pressure will aid in the design of novel, targeted drug therapies for treating kidney pathologies.
    Bioengineering Conference, 2004. Proceedings of the IEEE 30th Annual Northeast; 05/2004