--  Department of Environmental Medicine  --
PhD Admissions/Financial Aid Postdoctoral Opportunities
  Current Students   PhD Curriculum   Awards   Tox Seminars
    PhD Graduates: 2000–2010     Career Options
Fall Picnics-2010     2009     2008     2007     2006     2005     2004     2003     2002     2001 Tox Retreats-2010     2009     2008     2007     2006     2005     2004 Alumni Receptions-2010     2009     2008     2007     2006     2005     2004     2003     2002     2001 ATS Alumni Reception-2009 Life in Rochester
University of Rochester Medical Center School of Medicine Dept. of Environmental Medicine Other Basic Science PhD Programs UR Career Center: Info for Postdocs Life in Rochester
Dept. Environmental Medicine Home       — Toxicology PhD Home       — EHS Center Home
Environmental Medicine Faculty EHSC Faculty Tox PhD Program Faculty

Ph.D. Program in Toxicology

Recent Student Publications

   Every month the toxicology graduate students choose to honor a publication by one of their peers. The sixth “publication of the month,” chosen in early March 2012, was by Isaac K. Sundar, a postdoctoral student:
Sundar IK, Hwang JW, Wu S, Sun J, Rahman I. (2011) Deletion of vitamin D receptor leads to premature emphysema/COPD by increased matrix metalloproteinases and lymphoid aggregates formation. Biochem Biophys Res Commun. 406:127-133
“Vitamin D deficiency is linked to accelerated decline in lung function, increased inflammation, and reduced immunity in chronic lung diseases, such as asthma, cancer, and Chronic Obstructive Pulmonary Disease (COPD). Epidemiological studies have suggested that vitamin D insufficiency is associated with low lung function in susceptible subjects who are exposed to higher levels of environmental particulates/inhaled toxicants. The American Academy of Pediatrics reported the revised guidelines for vitamin D intake as 400 IU per day for healthy infants/children and 2000 IU for adolescents. Newer reports also support the potential role for vitamin D in maintaining innate immunity and in the prevention of chronic diseases including asthma, diabetes and cancer. Individuals with vitamin D deficiency/insufficiency will be more susceptible to chronic diseases. The mechanism of beneficial effects of vitamin D is unclear. [more]

(For more information on vitamin D and its role in chronic lung diseases, see this review: Sundar IK, Rahman I. Vitamin D and susceptibility of chronic lung diseases: role of epigenetics. Front Pharmacol. 2011; 2:50.)
   The fifth “publication of the month,” was by Bethany Winans. Environmental toxicants and the developing immune system: a missing link in the global battle against infectious disease? Winans B, Humble MC, and B. Paige Lawrence. Reprod Toxicol. 2011 Apr;31(3):327-336.

“There is now compelling evidence that in utero and early life exposure to pollutants can negatively impact health later in life. The early life environment has been shown to contribute to diseases such as cancer and obesity; less well studied is how early life environmental insults can impact the immune system. Given that the immune system is the body‘s first line of defense against invading pathogens, it is critical to understand how immune function may be altered by early life exposures. This review summarizes data that investigates how a number of pollutants, such as cigarette smoke and dioxin-like compounds, lead to changes in immune function in animal models. These data support the idea that developmental exposure to pollutants may persistently reduce immune function. Infectious diseases remain among the top five causes of death worldwide, and the findings reviewed here suggest that exposure to common chemicals from our daily environment may be an overlooked factor that contributes to this global burden of disease.”

This article by David H. McMillan, was the the fourth chosen as “publication of the month.” 		Lung-targeted overexpression of the NF-kB member ReIB dampens cigarette smoke-induced inflammation. McMillan DH, Baglole CJ, Thatcher TH, Maggirwar S, Sime PJ, and Phipps RP. Am J Pathol. 2011 Jul;179(1):125-133. “Acute lung inflammation can be caused by a variety of respirable agents, including cigarette smoke. Long-term cigarette smoke exposure can cause chronic obstructive pulmonary disease (COPD), a serious illness that affects >10 million Americans. Cigarette smoke is a known inducer of inflammation and is responsible for approximately 90% of all COPD cases. RelB, a member of the NF-kB family, attenuates cigarette smoke-induced inflammatory mediator production in mouse lung fibroblasts in vitro. We hypothesized that overexpression of RelB in the airways of mice would dampen acute smoke-induced pulmonary inflammation.

This article by Ming Kung, who recently presented his Ph.D. thesis defense, was chosen to be the third “student publication of the month.”. ß		 Aryl Hydrocarbon Receptor-Mediated impairment of chondrogenesis and fracture healing by cigarette smoke and benzo(a)pyrene. Kung MH, Yukata K, O’Keefe RJ, and Zuscik MJ. J. Cell Physiol. 2011 May 12. doi: 10.1002/jcp.22819.

“The clinical literature strongly suggests that bone healing in cigarette smokers is impaired.  Despite much effort, the molecular mechanisms underlying these effects are poorly understood.  Because cigarette smoke (CS) contains numerous polycyclic aromatic hydrocarbons (PAHs), and since dioxins impair bone formation in vivo via the Aryl Hydrocarbon Receptor (AHR), we hypothesized that PAHs in smoke exert deleterious effects on fracture repair through activation of the AHR.  We confirmed that the AHR is rapidly activated at the site of a fracture after a single exposure to cigarette smoke--thus establishing the possibility that PAHs in smoke exert direct effects on cells involved in fracture repair. ”
Melissa Badding’s publication was the second to be selected for this page.

Transcription   factor plasmid binding modulates microtubule interactions and   intracellular trafficking during gene transfer. Badding MA, Vaughan EE, and Gene Therapy. 2011 Jul 21. doi: 10.1038/gt.2011.113.

“For non-viral gene delivery to be successful, plasmids must move through the cytoplasm to the nucleus in order to be transcribed. While the cytoskeletal meshwork acts as a barrier to plasmid DNA movement in the cytoplasm, the microtubule network is required for directed plasmid trafficking to the nucleus. We have shown previously that plasmid-microtubule interactions require cytoplasmic adapter proteins such as molecular motors, transcription factors (TFs) and importins.” [more]
Sarah Latchney’s article was selected by vote of her peers to be first of this series.
Neural precursor cell proliferation is disrupted through activation of the aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Latchney SE, Lioy DT, Henry EC, Gasiewicz TA, Strathmann FG, Mayer-Pröschel M, and Opanashuk LA. Stem Cells Dev. 2011 Feb;20(2):313-326.

“The developing nervous system is highly susceptible to environmental insults because embryonic brain maturation is dictated by several waves of neurogenesis. Neurogenesis involves the proliferation of multipotent neural stem cells (NSC) followed by differentiation into lineage-restricted neural precursor cells (NPC) during the embryonic period.” [more].
Revised February 13 2012 (vgl & gbi)