Recent trends in the incidence of testicular germ cell tumors in the United States.

Testicular germ cell tumors (TGCT), which comprise 98% of all testicular malignancies, are the most commonly occurring cancers among men between the ages of 15 and 44 years in the United States (US). A prior report from our group found that while TGCT incidence among all US men increased between 1973 and 2003, the rate of increase among black men was more pronounced starting in 1989-1993 than was the rate of increase among other men. In addition, TGCT incidence increased among Hispanic white men between 1992 and 2003. To determine whether these patterns have continued, in the current study, we examined temporal trends in incidence through 2011. Between 1992 and 2011, 21 271 TGCTs (12 419 seminomas; 8715 non-seminomas; 137 spermatocytic seminomas) were diagnosed among residents of the Surveillance, Epidemiology, and End Results 13 registry areas. The incidence of TGCT was highest among non-Hispanic white men (6.97 per 100 000 man-years) followed by American Indian/Alaska Native (AI/AN; 4.66), Hispanic white (4.11), Asian/Pacific Islander (A/PI; 1.95), and black (1.20) men. Non-Hispanic white men were more likely to present with smaller tumors (3.5 cm) and localized disease (72.6%) than were men of other races/ethnicities. Between 1992 and 2011, TGCT incidence increased significantly among Hispanic white [annual percent change (APC) = 2.94, p < 0.0001], black (APC = 1.67, p = 0.03), non-Hispanic white (APC = 1.23, p < 0.0001), and A/PI (APC = 1.04, p = 0.05) men. Incidence rates also increased, although not significantly, among AI/AN men (APC = 2.96, p = 0.06). The increases were greater for non-seminoma than seminoma. In summary, while non-Hispanic white men in the US continue to have the highest incidence of TGCT, they present at more favorable stages of disease and with smaller tumors than do other men. The increasing rates among non-white men, in conjunction with the larger proportion of non-localized stage disease, suggest an area where future research is warranted.

Memory of past exposure to the chemokine IL-8 inhibits the contraction of fibroblast-populated collagen lattices.

The inflammatory cytokine makeup of healing wounds helps delineate the phases of the repair process. As an example, during the lag phase (inflammatory phase) of repair, elevated levels of IL-8, a chemokine, participate in the activation and chemotaxis of neutrophils. During the normal proliferative and remodeling phases of repair, IL-8 levels are minimal. Healing burn wounds often have small, open, slow-to-heal areas, which have been shown to contain elevated levels of IL-8. Does a limited exposure of IL-8 to fibroblasts in vitro at the concentrations measured in these unhealed sites cause altered cell behavior? To study this possibility the fibroblast-populated collagen lattice (FPCL) model, an in vitro model of wound contraction, was used to investigate fibroblast response to IL-8. As previously reported, the chronic exposure of fibroblasts to IL-8 at 30 ng/ml within FPCLs significantly inhibited FPCL contraction. Fibroblasts in monolayer culture were incubated with IL-8 for 3 days. In the absence of IL-8, FPCLs were manufactured with these preexposed cells and it was found that FPCL contraction was inhibited. Fibroblasts retained their reduced capacity of reorganizing collagen fibrils when previously exposed to IL-8. Treating fibroblasts in monolayer with IL-8 for only 1 h prior to their incorporation into collagen lattices caused inhibition of FPCL contraction. The speculation is that in vivo open areas in reepithelialized healed burns are the consequence of the local population of fibroblasts having been exposed to elevated levels of IL-8. Such an earlier exposure triggers a memory in this population of fibroblasts that alters their capacity to lay down an extracellular matrix that optimizes the migration of epidermal cells.

Effects of nimodipine and nicergoline on cerebrovascular injuries induced by activation of platelets and leukocytes in vivo.

Cerebral ischemia was induced in rabbits by selective injection of 4 beta-phorbol-12 beta-myristate-13 alpha-acetate (PMA) into the left carotid artery. PMA provoked intravascular platelet and neutrophil aggregation. After PMA injection, a significant decrease in platelet and neutrophil counts was observed. Platelet and neutrophil emboli caused ischemia of the brain and brain barrier damage with accumulation of sodium fluorescein in the cerebrospinal fluid. Regional tissue analysis showed an ipsilateral alteration of the cerebral energy state and increased lactate levels. Pretreatment with the prostacyclin infusion completely blocked the alterations in both platelet and leukocytes counts and decreased the cerebral energy failure. Nimodipine administration decreased the changes in platelet and neutrophil counts and prevented the development of both brain barrier and cerebral energy failure. Nicergoline had no statistically significant beneficial effect on PMA-induced cerebrovascular injury.