Lampson took the news with a teenager’s instincts: He jumped on the internet to research his disease.
“I never dwelled on the possibility of death. So I think ultimately that helped me because my immediate response was, ‘What do I do to beat it?’ ” Lampson said. “I never really grasped the gravity of having a cancer diagnosis.”
Even after learning the cancer had spread through his chest — years later he found out such cases had about a 65 percent five-year survival rate — Lampson still made the trip from his Hilliard, Ohio, home to Iowa for his club soccer team’s regional tournament. The next day, he began an aggressive chemotherapy regimen, which is no longer used, at Nationwide Children’s Hospital in Columbus.
The drugs attacked the cancer, and the experience sapped Lampson’s youthful innocence.
“It took an incredibly large toll on me as a person,” said Lampson, who had to put college on hold. “Obviously at 17 years old, everybody graduates high school. Everybody else goes on with their lives. So you find out who really loves you very quickly. … I got incredibly cynical. I started to hate everything.”
Fig 6. Cardiac remodeling in chagasic mice (± PARP1).
Mice (WT, PARP1+/-, and PARP1-/-) were infected with T. cruzi, and sacrificed at 150 days’ pi. (A-E) Cardiac structural changes were analyzed by echocardiography using a Vevo 2100 System. Shown are left ventricular (LV) mass (A), and systolic (-s) and diastolic (-d) changes in the thickness of the interventricular septum (IVS, B&C) and LV posterior wall (LVPW, D&E) in chronically infected and matched control mice (n = 8–12 mice/group, triplicate recordings per mouse). (F-H) Hearts were sectioned for various experiments as shown in G. Apex heart sections were stained with Mason’s trichrome, and representative images are shown in H.a-f. Tissue sections were scored for collagen (F, n = 4 mice/group, 2 slides per mouse, 10 microscopic fields per slide) as described in Materials and Methods. (I-K) Real time RT-qPCR analysis of myocardial levels of mRNAs for collagen isoforms COLI, COLIII, and COLV, in chronically infected (and control) WT, PARP1+/-, and PARP1-/- mice (n ? 5 mice/group, triplicate observations per mouse). Data were normalized to GAPDH mRNA. Data in all bar graphs are plotted as mean value ± SEM, and statistical significance are marked as *WT.Tc vs. WT, &genetically modified/infected vs. matched controls, and #WT.Tc vs. genetically-modified/infected (*,&,#p<0.05, **,##p<0.01, ***p<0.001).
The indices of LV systolic function, i.e., stroke volume (SV), cardiac output (CO), and ejection fraction (EF), were decreased by 66%, 51% and 46% respectively, in WT.Tc (vs. WT) mice (Fig 7A–7C, all, p<0.01). The systolic dysfunction prolonged the pre-ejection isovolumic contraction time (IVCT, 74% increase, Fig 7D, p<0.05) and shortened the LV ejection time (LVET, Fig 7E, p<0.05) in chagasic mice. Further, 40–67% changes in the early (E) and late (A) diastolic filling velocities indicated diastolic dysfunction in chagasic WT mice (Fig 7F & 7G, all, p<0.05). Both systolic and diastolic dysfunction contribute to abnormality in myocardial relaxation that was presented by 50% increase in isovolumic relaxation time (IVRT, Fig 7H, p<0.05) in WT.Tc mice. In comparison to WT.Tc mice, PARP1+/-.Tc and PARP1-/-.Tc mice exhibited a partial-to-full control of systolic and diastolic dysfunction, and myocardial contraction and relaxation indices, the maximal benefits of PARP1 deletion being observed in PARP1-/- mice (Fig 7A–7H).