Last week our lab came together in the Clinical Research Unit at the University of Iowa to film the online supplement to our paper titled “Combining volumetric capnography and barometric plethysmography to measure the lung structure-function relationship.” This method allows the investigator to measure the volume of the airways at different lung volumes, to more comprehensively evaluate the lung. As we say in the paper…
This may be a valuable tool for investigators aiming to quantify the influence of airways mechanics versus lung compliance and elastance on pulmonary function in healthy and diseased populations. Furthermore accounting for the absolute lung volume at which the… measurements are being performed allows investigators to characterize the effects of conditions that can alter the inflation state of the lung, such as obesity, lung transplant, or interventions like chest wall strapping. [This method] may ultimately have clinical utility in the intensive care setting.
The paper is in-press with the Journal of Visualized Experiments and will be available soon. Thanks to our collaborators and lab members who came out and contributed to the process!
Today members of the lab took a momentary break from the daily grind of research to celebrate Halloween. Each lab member seems to have independently chosen a scientist-type get-up, with Professor Bates and grad student Hannah choosing a Rick and Morty themed outfit. Hannah, however, truly paid homage to the new cult class by bringing her own Morty as an accessory. Rotating Ph.D. student Adam shined as Bill Nye and Professor Tomasson stretched beyond his comfort zone and dressed as a physician scientist.
A focus of our laboratory is understanding the regulation of pulmonary blood vessels by hypoxia, including non-canonical intrapulmonary shunt vessels. While we still don’t understand a lot about their structure, we recently found that they are regulated (in part) by the beta-2 adrenergic pathway. Beta-2 adrenergic receptors cause dilation (or widening) of blood vessels in the body. Blocking these receptors prevents intrapulmonary shunt vessels from being fully recruited. This is important because opening these pathways may compromise oxygen uptake, which is a major function of the lung.
There is a lot about these pathways that we still don’t understand. Our current interest is motivated by their identification in the lungs of infants and adults that have died of pulmonary hypertension. We hope that by studying their regulation, we can better understand the role they play in lung disease and develop new treatments for these patients.
We are pleased to announce that we have received a one-year, $60,000 seed grant to examine the environmental and genetic determinants underlying the transition of of MGUS into multiple myeloma. MGUS is a precursor, pre-malignant condition that occurs before the development of multiple myeloma. The majority of MGUS cases are benign, but can be devastating when it develops into multiple myeloma. Risk factors for MGUS and myeloma are age, sex, race and obesity and there is currently no cure for myeloma. In a collaboration with Dr. Gail Bishop, we will use these funds to investigate the causes behind malignant transformation. Based on a theory advanced by Dr. Bates, we will investigate a potential association between myeloma and sleep apnea. The short-term goal of this collaborative effort is to determine the effect of intermittent hypoxia on the immune system and on pre-malignant plasma cells.
As a National Cancer Institute-designated comprehensive cancer center, the Holden Comprehensive Cancer Center at the University of Iowa is empowered to fund a variety of mission-aligned developmental research projects (such as this one) through its NCI award. Every comprehensive cancer center including the University of Iowa’s HCCC stresses the importance of multidisciplinary approaches in research and care, ensuring greater productivity and a faster translation of discoveries into more effective treatments.
Work completed with our collaborators in Naomi Chesler’s laboratory has been accepted for publication in the Journal of Biomechanics! The paper titled “Pulmonary arterial strain- and remodeling-induced stiffening are differentiated in a chronic model of pulmonary hypertension ” reports our finding that chronic thromboembolic pulmonary hypertension causes stiffening of the large elastic arteries and that this is correlated with changes in their structure.
Pulmonary hypertension is high blood pressure in the lung vessels that can ultimately lead to heart failure. There is currently no cure for pulmonary hypertension and the prognosis for these patients is pretty grim. 66% of patients die within five years of their diagnosis. Understanding the factors that contribute to the development of pulmonary hypertension will hopefully lead to new treatments for this devastating.