Water Loss and Desiccation Tolerance of the Two Yearly Generations of Adult and Nymphal Kudzu Bugs, Megacopta cribraria (Hemiptera: Plataspidae).

Water loss rate, percentage total body water content (%TBW), cuticular permeability (CP), and desiccation tolerance were investigated in adult and immature stages of the invasive kudzu bug, Megacopta cribraria (Fab.) (Hemiptera: Plataspidae), a serious soybean pest and an urban nuisance. Adults and all five nymphal instars were weighed prior to and 2, 4, 6, 8, 10, and 24 h after desiccated at 30 ± 1°C and 0-2% RH. Both % initial mass and %TBW loss increased linearly with time of desiccation. Rates of loss ranged from approximately 1-7%/h. Mortality occurred at 10 h after desiccation. Desiccation tolerance (%TBW lost at death) ranged between 25.6% for first-generation adult females and 75% for first-generation fifth-instar nymphs. First-generation first-instar nymphs had significantly greater %TBW (88.9%) than the other generations and instars, whereas second-generation fifth instars had the lowest %TBW (62.4%). The CP value of first-generation adult females (12.3 ± 1.6 µg cm-1 h-1 mmHg-1) was the greatest across generations. First-generation first instars had the greatest mass loss (111.11 mg/g) among all instars and generations, whereas overwintered second-generation adult females had the lowest mass loss (18.39) across generations. This study demonstrated that desiccation stress differentially affected the survival of adult and nymphal kudzu bugs and may imply that environmental stress can affect the relative abundance of this species in the fields and around homes.

Leukocyte matrix metalloproteinase-9 is elevated and contributes to lymphocyte activation in type I diabetes.

Degradation of extracellular matrix proteins by matrix metalloproteinases (MMPs) is integral to cell migration and tissue remodeling in diabetes mellitus and its complications. MMPs also regulate the function of leukocytes via proteolytic processing of cytokines/chemokines. In this study, we measured the production of MMP-9 and its natural tissue inhibitor (TIMP)-1 by leukocytes isolated from human type I diabetic patients. MMP-9 was also detected in serum and splenocytes from non-obese diabetic (NOD) and BALB/c mice. MMP-9 was markedly elevated in leukocytes from diabetics compared to non-diabetic controls. TIMP-1 production was also enhanced in leukocytes from diabetics, but substantially less than MMP-9, with the MMP-9/TIMP-1 ratio being 1.6-fold higher in neutrophils and 3-fold higher in monocytes than controls. Interleukin (IL)-2 or lipopolysaccharide (LPS) treatment increased MMP-9 production in leukocytes from both diabetics and normal controls, whereas insulin decreased MMP-9 expression. Recombinant MMP-9 stimulated the proliferation of mouse splenocytes from NOD or BALB/c and a MMP-9 inhibitor dose-dependently inhibited splenocyte proliferation. In conclusion, our results demonstrate firstly that MMP-9 expression is elevated in leukocytes from type I diabetic patients and NOD mice and secondly, that MMP-9 elevates proliferation of mouse splenocytes. These data suggest that elevated leukocyte MMP-9 may contribute to the pathogenesis of type I diabetes and its associated complications.