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From 1998 to 2008, 68 adult female loggerhead sea turtles (Caretta caretta) were instrumented with platform transmitter terminals at nesting beaches in Georgia, North Carolina (NC) and South Carolina (SC) on the East Coast of the United States of America (30°48'N, 81°28'W to 33°51'N, 77°59'W). The majority of post-nesting loggerheads (N = 42, 62 %) migrated to foraging habitats in the Mid-Atlantic Bight during May-October, with a subsequent migration occurring during November-March to foraging habitats south of Cape Hatteras, NC. Nine (13 %) loggerheads initially foraged in the near-shore, coastal areas of the South Atlantic Bight, but moved to offshore habitats--closer to the Gulf Stream--during November-March, while fourteen (21 %) loggerheads remained in foraging areas along the mid-continental shelf off of the eastern coast of Florida and/or continued southward to Florida Bay and the Bahamas. The present study delineates important, post-nesting foraging habitats and migration corridors where loggerheads may interact with commercial fisheries--providing managers opportunities to develop and implement optimally effective conservation actions for the recovery of this threatened species., Introduction Global loggerhead sea turtle (Caretta caretta) populations are considered to be declining (NMFS and USFWS 2007). As a result, loggerheads are listed as Endangered on the IUCN Red List [...]

Airway smooth muscle (ASM) from infant guinea pigs has less spontaneous relaxation during stimulation than ASM from adults. Inhibition of cyclooxygenase (COX), which catalyzes the production of prostanoids, increases this relaxation in infant ASM and abolishes age differences, thus suggesting that prostanoids reduce relaxation in infant ASM. In this study, we investigated whether leukotrienes are also involved in reducing spontaneous relaxation; whether the two COX isoforms, COX-1 and COX-2, differentially regulate spontaneous relaxation; and whether prostanoid release is developmentally regulated in guinea pig ASM. In different age groups, we measured relaxation during and after electrical stimulation in tracheal strips as well as prostanoid release from tracheal segments. Relaxation was studied in the absence and in the presence of a lipoxygenase inhibitor, a cysteinyl leukotriene receptor-1 antagonist, a COX-1 inhibitor, or a COX-2 inhibitor. We found that inhibition of lipoxygenase or cysteinyl leukotriene receptor-I antagonism did not increase spontaneous relaxation at any age, thus excluding a role for leukotrienes in this phenomenon. Inhibition of COX-2, but not COX-1, promoted spontaneous relaxation. The basal release of prostanoids was more abundant in tissue from infant animals and decreased significantly with age. Thromboxane [B.sub.2] was the most abundant metabolite released at all ages. Electrical stimulation and epithelium removal did not affect the age difference in prostanoid release. We conclude that increased basal prostanoid release contributes to the reduced spontaneous relaxation in immature guinea pig ASM compared with older animals. By regulating ASM relaxation, prostanoids may play a role in the airway hyperresponsiveness at a young age. airway hyperresponsiveness; bronchospasm removal; cyclooxygenase; lipoxygenase; ontogenesis

NAD(P)H oxidase is one of the critical enzymes mediating cellular production of reactive oxygen species and has a central role in airway smooth muscle (ASM) cell proliferation. Since reactive oxygen species also affect ASM contractile response, we hypothesized a regulatory role of NAD(P)H oxidase in ASM contractility. We therefore studied ASM function in wild-type mice (C57BL/6J) and mice deficient in a component ([p47.sup.phox]) of NAD(P)H oxidase. In histological sections of the trachea, we found that the area occupied by ASM was 17% more in [p47.sup.phox-/-] than in wild-type mice. After correcting for the difference in ASM content, we found that force generation did not vary between the two genotypes. Similarly, their ASM shortening velocity, maximal power, and sensitivity to acetylcholine, as well as airway responsiveness to methacholine in vivo, were not significantly different. The main finding of this study was a significantly reduced ASM relaxation in [p47.sup.phox-/-] compared with wild-type mice both during the stimulus and after the end of stimulation. The tension relaxation attained at the 20th second of electric field stimulation was, respectively, 17.6 [+ or -] 2.4 and 9.2 [+ or -] 2.3% in null and wild-type mice (P < 0.01 by t-test). Similar significant differences were found in the rate of tension relaxation and the time required to reduce tension by one-half. Our data suggest that NAD(P)H oxidase may have a role in the structural arrangement and mechanical properties of the airway tissue. Most importantly, we report the first evidence that the [p47.sup.phox] subunit of NAD(P)H oxidase plays a role in ASM relaxation. airways; airway responsiveness; contractility; reactive oxygen species

Abstract: Evidence for contributions of airway smooth muscle (ASM) to the hyperresponsiveness of newborn and juvenile airways continues to accumulate. In our laboratory, 3 novel paradigms of hyperresponsiveness of newborn [...]

Transforming growth factor-[beta]1 (TGF-[beta]1) plays a pivotal role in increasing airway smooth muscle mass in severe asthma by inducing proliferation and hypertrophy of human airway smooth muscle. The mechanism(s) for these effects of TGF-[beta]1 have not been fully elucidated. In this study, we demonstrate that TGF-[beta]1 is a potent inducer of expression of the nonphagocyte NAD(P)H oxidase catalytic homolog Nox4, diphenylene iodonium-inhibitable reactive oxygen species production, proliferation, and hypertrophy in cultured human airway smooth muscle cells. By confocal microscopy, TGF-[beta]1-induced Nox4 was localized with the endoplasmic reticulum and the nucleus, implying a role for Nox4 in regulation of both the cell cycle and protein synthesis. Consistent with this hypothesis, TGF-[beta]1 increased retinoblastoma protein phosphorylation at both Ser807/811 and Ser780. Silencing Nox4 prevented TGF-[beta]1-mediated retinoblastoma protein phosphorylation, proliferation, and cell hypertrophy. TGF-[beta]1 also increased phosphorylation of eukaryotic translation initiation factor 4E binding protein-1 at Thr37/46, and this was likewise blocked by silencing Nox4. This is the first report to suggest a functional role for Nox4 in cell cycle transition and to demonstrate that Nox4 influences the pathobiochemistry of asthma by generating reactive oxygen species that promote TGF-[beta]1-induced proliferation and hypertrophy of human airway smooth muscle. Myc; cdc2; eukaryotic translation initiation factor 4E binding protein- 1; nicotinamide adenine dinucleotide phosphate oxidase; reactive oxygen species; translation doi: 10.1152/ajplung.00430.2006

Deep inspiration counteracts bronchospasm in normal subjects but triggers further bronchoconstriction in hyperresponsive airways. Although the exact mechanisms for this contrary response by normal and hyperresponsive airways are unclear, it has been suggested that the phenomenon is related to changes in force-generating ability of airway smooth muscle after mechanical oscillation. It is known that healthy immature airways of both humans and animals exhibit hyperresponsiveness. We hypothesize that the profile of active force generation after mechanical oscillation changes with maturation and that this change contributes to the expression of airway hyperresponsiveness in juveniles. We examined the effect of an acute sinusoidal length oscillation on the force-generating ability of tracheal smooth muscle from 1 wk, 3 wk, and 2- to 3-mo-old guinea pigs. We found that the length oscillation produced 15-20% initial reduction in active force equally in all age groups. This was followed by a force recovery profile that displayed striking maturation-specific features. Unique to tracheal strips from 1-wk-old animals, active force potentiated beyond the maximal force generated before oscillation. We also found that actin polymerization was required in force recovery and that prostanoids contributed to the maturation-specific force potentiation in immature airway smooth muscle. Our results suggest a potentiated mechanosensitive contractile property of hyperresponsive airway smooth muscle. This can account for further bronchoconstriction triggered by deep inspiration in hyperresponsive airways. actin polymerization; deep inspiration; hyperresponsive airways; ontogenesis; prostanoids

Previously, we showed the shortening velocity of guinea pig tracheal strips was the greatest in juvenile (3-wk-old) compared with infant (1-wk-old) and adult animals (3-mo-old). The greatest shortening velocity was associated with the least resistance to shortening calculated from force-velocity curves among the three age groups. It remained to be verified if the stiffness of tracheal tissue, a measure of tissue response to geometrical deformations, is different among the three age groups. We hypothesized that stiffness of intact tracheal strips is lowest in the juvenile group and that this can explain the ontogeny of airway smooth muscle resistance to shortening and shortening velocity. Static stiffness measured through stepwise deformations showed no age-related differences. Evaluation of tissue response to oscillatory deformations showed that the dynamic stiffness of unstimulated tracheal strips was 8.35 [+ or -] 0.88, 4.15 [+ or -] 1.09, and 8.21 [+ or -] 1.57 kPa, and the phase angle was 10.3 [+ or -] 2.93, 2.46 [+ or -] 0.67, and 7.87 [+ or -] 1.77[degrees] in infant, juvenile, and adult, respectively. Unstimulated juvenile strips were significantly lower in dynamic stiffness and phase angle compared with unstimulated infant or adult strips. This maturational profile was independent of muscle strip preset length or oscillation mode/amplitude but was abolished at peak of contraction to either carbachol or electric field stimulation. These results suggest that the noncontractile components of tracheal strips are less stiff and contain fewer viscous/frictional elements in juvenile than in other age groups. This may provide a functional basis for reduced resistance to length changes in juvenile airway smooth muscle. ontogenesis; viscoelasticity

Evidence is rapidly accumulating that low-activity-reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases homologous to that in phagocytic cells generate reactive oxygen species as signaling intermediates in both endothelium and vascular smooth muscle. We therefore explored the possibility of such an oxidase regulating growth of airway smooth muscle (AWSM). Proliferation of human AWSM cells in culture was inhibited by the antioxidants catalase and N-acetylcysteine, and by the flavoprotein inhibitor diphenylene iodonium (DPI). Membranes prepared from human AWSM cells generated superoxide anion ([O.sup.-.sub.2]) measured by superoxide dismutase-inhibitable lucigenin chemiluminescence, with a distinct preference for NADPH instead of reduced nicotinamide adenine dinucleotide as substrate. Chemiluminescence was also inhibited by DPI, suggesting the presence of a flavoprotein containing oxidase generating ([O.sup.-.sub.2]) as a signaling molecule for cell growth. Examination of human AWSM cells by reverse transcriptase-polymerase chain reaction consistently demonstrated transcripts with sequences identical to those reported for [p22.sup.phox]. Transfection with p22phox antisense oligonucleotides reduced human AWSM proliferation. Inhibition of NADPH oxidase activity with DPI prevented serum-induced activation of nuclear factor-[kappa]B (NF-[kappa]B), and overexpression of a superrepressor form of the NF-[kappa]B inhibitor I[kappa]B[alpha] significantly reduced human AWSM growth. These findings suggest that an NADPH oxidase containing [p22.sup.phox] regulates growth-factor responsive human AWSM proliferation, and that the oxidase signals in part through activation of the prototypical redox-regulated transcription factor NF-[kappa]B. superoxide anion; diphenylene iodonium; [p22.sup.phox]

Abstract Blood samples were obtained from 38 wild red deer (Cervus elaphus) at two sites in Ireland and subjected to PCR analysis of the 18S rRNA gene followed by sequencing. Two fragments of the 18S rRNA gene were generated by two different PCR protocols and subsequent sequencing suggested that at least six of the deer were infected by a babesia that, in those loci, is indistinguishable from Babesia divergens, an important tick-borne pathogen of cattle and of zoonotic significance. Additionally, a B. odocoilei-like parasite was detected in three samples and a babesia that did not match any sequences in the GenBank database was found in five samples. Neither B. capreoli nor B. venatorum (EU1) were found. There have been several reports of B. divergens occurring in deer species, including red deer, roe deer (Capreolus capreolus) and reindeer (Rangifer tarandus). However, in view of recent re-sequencing of bovine-origin samples deposited previously in GenBank, it is unlikely that any of these sequences from deer are B. divergens. The present study describes the only deer piroplasm detected so far that shows complete identity with B. divergens, in just over half of the 18S rRNA gene. The entire gene of this deer parasite should be analysed and transmission experiments undertaken before the infectivity of B. divergens for red deer can be confirmed.

Cryptosporidium spp. was detected in 25 of 56 pig slurry samples from 33 Irish farms by PCR and DNA sequencing. Results revealed that Cryptosporidium oocysts could persist in treated slurry and potentially contaminate surface water through improper discharge or uncontrolled runoff.