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PubMed2006

The role of Toll-like receptors in non-infectious lung injury.

The role of Toll-like receptors (TLRs) in pathogen recognition has been expeditiously advanced in recent years. However, investigations into the function of TLRs in non-infectious tissue injury have just begun. Previously, we and others have demonstrated that fragmented hyaluronan (HA) accumulates during tissue injury. CD44 is required to clear HA during tissue injury, and impaired clearance of HA results in unremitting inflammation. Additionally, fragmented HA stimulates the expression of inflammatory genes by inflammatory cells at the injury site. Recently, we identified that HA fragments require both TLR2 and TLR4 to stimulate mouse macrophages to produce inflammatory chemokines and cytokines. In a non-infectious lung injury model, mice deficient in both TLR2 and TLR4 show an impaired transepithelial migration of inflammatory cells, increased tissue injury, elevated lung epithelial cell apoptosis, and decreased survival. Lung epithelial cell overexpression of high molecular mass HA protected mice against acute lung injury and apoptosis, in part through TLR-dependent basal activation of NF-kappaB. The exaggerated injury in TLR2 and TLR4 deficient mice appears to be due to impaired HA-TLR interactions on epithelial cells. These studies identify that host matrix component HA and TLR interactions provide signals that initiate inflammatory responses, maintain epithelial cell integrity, and promote recovery from acute lung injury.

Animals↗
PubMedDate not supplied

Brain fibronectin expression in prenatally irradiated mice.

Activation of gene transcription by radiation has been recently demonstrated in vitro. However, little is known on the specificity of these alterations on gene transcription. Prenatal irradiation is a known teratogen that affects the developing mammalian central nervous system (CNS). Altered neuronal migration has been suggested as a mechanism for abnormal development of prenatally irradiated brains. Fibronectin (FN), an extracellular glycoprotein, is essential for neural crest cell migration and neural cell growth. In addition, elevated levels of FN have been found in the extracellular matrix of irradiated lung. To test whether brain FN is affected by radiation, either FN level in insoluble matrix fraction or expression of FN mRNA was examined pre- and postnatally after irradiation. Mice (CD1), at 13 d of gestation (DG), served either as controls or were irradiated with gamma rays at 0.5 or 1 Gy. Control and irradiated animals were killed either at 13 DG, 14 DG, 17 DG, or 5, 6, or 14 d postnatal. Brain and liver were collected from offspring and analyzed for either total FN protein levels or relative mRNAs for FN and tubulin. Results of prenatal irradiation on reduction of postnatal brain weight relative to whole body weight and morphological reduction in cerebral cortex regions of postnatal brains are comparable to that reported by others. Insoluble matrix fraction (IMF) per gram of brain, liver, lung, and heart weight was not significantly different either between control and irradiated groups or between postnatal stages, suggesting that radiation did not affect the IMF. However, total amounts of FN in brain IMF at 17 DG were significantly different (p < .02) between normal (1.66 +/- 0.80 micrograms) and irradiated brains (0.58 +/- 0.22 microgram). FN mRNA was detectable at 13, 14, and 17 DG, but was not detectable at 6 and 14 d postnatal, indicating that FN mRNA is developmentally regulated. After 0.5 Gy of irradiation, expression of FN mRNA was reduced to 36% +/- 22% (1 h), 52% +/- 10% (1 d), and 76% +/- 10% (4 d) of the control level. After 1 Gy of irradiation, relative FN mRNA was 62% +/- 28% (1 h) and 75% +/- 3% (4 days) to the control level, respectively. This reduction was comparable to that reported by others for the cytoskeletal protein beta-actin. In contrast, mRNA for tubulin, another cytoskeletal protein, increased at 1 h after irradiation but then approached normal postnatally. The longer lasting alteration of FN may be more directly related to neural development, particularly if the reduction in FN is nonuniform.

Animals↗
PubMed1995

Parathyroid hormone and the cellular immune system.

Parathyroid hormone (PTH) is the main hormone controlling calcium concentration in the extracellular fluid (ECF) through its biological activity on bone, kidney and intestine. However, data published over the last two decades indicate that PTH may act as an immunomodulator. The purpose of the present review is to summarize the effects of PTH on various immune functions. Polymorphonuclear leukocytes of patients with chronic renal failure (CRF) and elevated blood levels of PTH showed impaired migration, reduced phagocytic and bactericidal activity, and inhibited granulocyte chemotaxis. Antibody production and T and B lymphocyte proliferation are affected by PTH, both in vivo and in vitro. Possible implications of the involvement of PTH and its fragments in CRF are discussed.

Animals↗
PubMedDate not supplied

Biological and social correlates of blood pressure among Japanese men in Hawaii.

A cohort of more than 8,000 Japanese men living in Hawaii was studied for factors associated with blood pressure levels, with an emphasis on biological and sociocultural variables. Bivariate and multivariate analyses of more than 50 variables indicated that obesity, age, hematocrit, heart rate, forced vital capacity, serum triglyceride, serum uric acid, cigarette consumption, and family history of hypertension were independently associated with both cross-sectional levels and longitudinal changes in blood pressure. Serum glucose and alcohol consumption were associated with cross-sectional levels only. There was little evidence of association for specific dietary items, type of diet, diet changes, or use of salt. Furthermore, there was no support for the psychosocial hypotheses of elevated blood pressure from the stress of migration, acculturation, or status incongruity.

Acculturation↗
PubMed1993

Inhibition of urokinase synthesis and cell surface binding alters the motile behavior of embryonic endocardial-derived mesenchymal cells in vitro.

The expression of the serine protease urokinase is elevated during the epithelial-mesenchymal transformation of the endocardium in the developing avian heart. Elevated urokinase expression is associated with the migrating mesenchymal cells of the atrioventricular canal and bulbotruncus and not the myocardium. Treatment of isolated endocardial-derived mesenchymal cells with phosphatidyinositol-specific phospholipase C released urokinase and its receptor from the cell surface and caused significant alterations in cell morphology and motility. Likewise inhibition of urokinase synthesis by treatment of cells with antisense oligonucleotides also inhibited the migration and motility of the endocardial-derived cells. These results suggest an important role for this enzyme in cell-matrix interactions and cell migration during development.

Animals↗
PubMed2003

Overexpression of Hsp27 in a human melanoma cell line: regulation of E-cadherin, MUC18/MCAM, and plasminogen activator (PA) system.

Hsp27 is considered a potential marker for cell differentiation in diverse tissues. Several aspects linked to the differentiation process and to the transition from high to low metastatic potential were analyzed in melanoma cells transfected with Hsp27. E-cadherin plays a central role in cell differentiation, migration, and normal development. Loss of expression or function of E-cadherin has been documented in a variety of human malignancies. We observed by fluorescence-activated cell sorter (FACS) as well as immunofluorescence (IF) analysis a pronounced expression of E-cadherin in Hsp27-transfected A375 melanoma cells compared with control melanoma cells. The expression of the adhesion molecule MUC18/MCAM correlates directly with the metastatic potential of melanoma cells. In contrast to wild-type and neotransfected melanoma cells, in Hsp27-transfected cells the expression of MUC18/MCAM could not be detected by FACS and IF analysis. The plasminogen activator (PA) system plays a central role in mediating extracellular proteolysis and also in nonproteolytic events such as cell adhesion, migration, and transmembrane signaling. Hsp27 transfectants revealed elevated messenger ribonucleic acid expression of the urokinase-type PA (uPA) and its inhibitor, PA inhibitor type 1, which might indicate a neutralization effect of the proteolytic activity of uPA. Control cells failed to express both these molecules. The influence of Hsp27 expression on uPA activity and the involvement of E-cadherin could be demonstrated by use of anti-E-cadherin-blocking antibody. Our data provide evidence for an inhibitory-regulatory role of Hsp27 in tumor progression as found in our system.

Antigens, CD↗
PubMed2006

CXCR4 chemokine receptor mediates prostate tumor cell adhesion through alpha5 and beta3 integrins.

The mechanisms leading to prostate cancer metastasis are not understood completely. Although there is evidence that the CXC chemokine receptor (CXCR) 4 and its ligand CXCL12 may regulate tumor dissemination, their role in prostate cancer is controversial. We examined CXCR4 expression and functionality, and explored CXCL12-triggered adhesion of prostate tumor cells to human endothelium or to extracellular matrix proteins laminin, collagen, and fibronectin. Although little CXCR4 was expressed on LNCaP and DU-145 prostate tumor cells, CXCR4 was still active, enabling the cells to migrate toward a CXCL12 gradient. CXCL12 induced elevated adhesion to the endothelial cell monolayer and to immobilized fibronectin, laminin, and collagen. Anti-CXCR4 antibodies or CXCR4 knock out significantly impaired CXCL12-triggered tumor cell binding. The effects observed did not depend on CXCR4 surface expression level. Rather, CXCR4-mediated adhesion was established by alpha5 and beta3 integrin subunits and took place in the presence of reduced p38 and p38 phosphorylation. These data show that chemoattractive mechanisms are involved in adhesion processes of prostate cancer cells, and that binding of CXCL12 to its receptor leads to enhanced expression of alpha5 and beta3 integrins. The findings provide a link between chemokine receptor expression and integrin-triggered tumor dissemination.

Cell Line, Tumor↗
PubMed2007

Mesenchymal stem cells regulate angiogenesis according to their mechanical environment.

In fracture and bone defect healing, MSCs largely drive tissue regeneration. MSCs have been shown to promote angiogenesis both in vivo and in vitro. Angiogenesis is a prerequisite to large tissue reconstitution. The present study investigated how mechanical loading of MSCs influences their proangiogenic capacity. The results show a significant enhancement of angiogenesis by conditioned media from mechanically stimulated compared with unstimulated MSCs in two-dimensional tube formation and three-dimensional spheroid sprouting assays. In particular, proliferation but not migration or adhesion of endothelial cells was elevated. Promotion of angiogenesis was dependent upon fibroblast growth factor receptor 1 (FGFR1) signaling. Moreover, stimulation of tube formation was inhibited by vascular endothelial growth factor receptor (VEGFR) tyrosine kinase blocking. Screening for the expression levels of different soluble regulators of angiogenesis revealed an enrichment of matrix metalloprotease 2, transforming growth factor beta1, and basic fibroblast growth factor but not of vascular endothelial growth factor in response to mechanical stimulation. In conclusion, mechanical loading of MSCs seems to result in a paracrine stimulation of angiogenesis, most likely by the regulation of a network of several angiogenic molecules. The underlying mechanism appears to be dependent on the FGFR and VEGFR signaling cascades and might be mediated by an additional cross-talk with other pathways.

Arthroplasty, Replacement, Hip↗
PubMedDate not supplied

Circadian distribution of hematology variables in subjects with multiple sclerosis.

Hematology variables were measured in blood samples obtained every 3h (8/24h) from 10 multiple sclerosis (MS) patients and 34 healthy subjects and analyzed for circadian characteristics using the population multiple-components method. Red blood cell (RBC) and hemoglobin levels as well as hematocrits exhibited circadian rhythms with minimal amplitudes in healthy individuals and insignificant variability in the smaller group of MS patients. In contrast the total white blood cell (WBC) and platelet counts for MS patients and healthy individuals both showed significant circadian characteristics while the mean 24h WBC and platelet levels did not significantly differ between the two groups. When the different WBC subsets were examined independently, statistically significant circadian rhythms were seen for lymphocytes and eosinophils for both MS patients and healthy individuals and for neutrophils only in the latter. Moreover, the 24h mean levels of lymphocytes, basophils, and eosinophils were significantly higher for the healthy controls while those of monocytes were higher for the MS patients. However, of all the variables tested with significant circadian rhythms in both groups of individuals, only those of lymphocyte numbers exhibited different patterns with somewhat higher amplitude in healthy individuals and a peak level occurring over an hour after that of MS patients. These changes may be the reflection of a disturbance in the regulation of patterns of lymphocyte activity and migration in MS patients. In addition, the elevation in circulating monocytes in MS patients is consistent with the inflammatory nature of the disease.

Adult↗
PubMed1986

[Disorders of immunologic homeostasis as affected by radioactive iodine preparations].

(CBA X C57B1/6)F1 mice were injected with 125I and 131I-sodium iodide at a dose of 5.74 X 10(4) Bq/g. For a long time after such treatment the animals manifested an increased level of spleen cells humoral immune response to a foreign antigen (sheep erythrocytes), the autoreactivity of spleen and lymph node lymphocytes to autologous erythrocytes was also elevated. At the same time the selective migration of 51Cr-labeled spleen lymphocytes to the peripheral lymphoid organs was suppressed. The use of a model system of adoptive cell transfer revealed an increase in the functional activity of cells suppressing a humoral response in mice treated with radiopharmaceuticals. The most pronounced disturbances of immunological reactivity in mice took place 6 mos. after the beginning of the experiment. The results obtained indicated that mechanisms of immune response regulation played a certain role in disturbances of immunological homeostasis induced by radioactive iodine agents.

Animals↗
PubMed2006

Costimulation of chemokine receptor signaling by matrix metalloproteinase-9 mediates enhanced migration of IFN-alpha dendritic cells.

Type I IFNs induce differentiation of dendritic cells (DCs) with potent Ag-presenting capacity, termed IFN-alpha DCs, that have been implicated in the pathogenesis of systemic lupus erythematosus. In this study, we found that IFN-alpha DCs exhibit enhanced migration across the extracellular matrix (ECM) in response to chemokines CCL3 and CCL5 that recruit DCs to inflammatory sites, but not the lymphoid-homing chemokine CCL21. IFN-alpha DCs expressed elevated matrix metalloproteinase-9 (MMP-9), which mediated increased migration across ECM. Unexpectedly, MMP-9 and its cell surface receptors CD11b and CD44 were required for enhanced CCL5-induced chemotaxis even in the absence of a matrix barrier. MMP-9, CD11b, and CD44 selectively modulated CCL5-dependent activation of JNK that was required for enhanced chemotactic responses. These results establish the migratory phenotype of IFN-alpha DCs and identify an important role for costimulation of chemotactic responses by synergistic activation of JNK. Thus, cell motility is regulated by integrating signaling inputs from chemokine receptors and molecules such as MMP-9, CD11b, and CD44 that also mediate cell interactions with inflammatory factors and ECM.

Animals↗
PubMed1999

Intracellular signals and cytoskeletal elements involved in oligodendrocyte progenitor migration.

We have examined the potential roles of intracellular Ca2+ regulation and of multiple cytoskeletal elements in control of the directed migration of cultured oligodendrocyte progenitor cells (OPs). OPs were found to migrate in response to platelet-derived growth factor (PDGF) or to a lesser extent to basic fibroblast growth factor (FGF) in a non-additive manner. This response was inhibited by chelation of intracellular Ca2+ by using BAPTA-AM. OP migration was not evoked by the neurotransmitter agonists phenylephrine or methacholine, which elevate OP Ca2+ levels. Inhibition of the MAP kinase pathway with PD 098059 did not affect OP migration to PDGF. Within growth cone-like leading edges of migratory OP processes, monomeric and filamentous actin were found to be colocalized with myosin and filamentous actin was prominent in filopodia extending beyond the leading edge. Tubulin was distributed throughout OP processes and cell bodies. Inhibition of actin or tubulin polymerization, by using cytochalasin B or nocodazole, respectively, altered OP morphology and markedly impaired migration. Inhibition of the myosin ATPase by BDM, which prevents force-generating actin/myosin interactions, greatly inhibited the chemotaxic response at concentrations that did not disrupt cell morphology. These results indicate that growth factors stimulate OP migration by activating pathways which include intracellular Ca2+ regulation, and characterize the distribution of multiple cytoskeletal elements involved in the generation of directed OP movement.

Animals↗
PubMed2000

High potassium intake inhibits neointima formation in the rat carotid artery balloon injury model.

Recently, we reported that elevated extracellular potassium concentration in vitro inhibited proliferation and migration of vascular smooth muscle cells, formation of free radical compounds by macrophages, and reduced platelet sensitivity to agonists. In the present study we analyzed the effects of long-term, in vivo elevation of extracellular potassium concentration resulting from changes in dietary potassium intake on the vascular response to injury. The rat carotid artery balloon injury model was employed in 70 adult Sprague Dawley rats assigned to three groups. Beginning 14 days before surgical placement of the carotid lesion and continuing until death, the animals were fed diets containing either low (0.1% potassium, n = 25), normal (1.5% potassium, n = 19), or high potassium (4.0% potassium, n = 26). Fourteen days postsurgery the animals were killed and the arteries were analyzed to determine quantitatively the ratio of neointimal to medial area. Dietary potassium had a significant effect on arterial plasma potassium concentration (one-way analysis of variance, P < .01). Group mean and standard errors were 4.26+/-0.12 mmol/L for the low-potassium group, 5.22+/-0.19 mmol/L for normal, and 5.80+/-0.23 mmol/L for the high-intake group. Increases in dietary potassium attenuated neointima formation significantly (P < .05, one-way analysis of variance), with the mean ratio of neointimal area to medial area being 0.447+/-0.106 for the low-intake animals, 0.384+/-.116 for normal, and 0.240+/-.046 for the high-intake group. These results are consistent with a hypothesis that a high level of potassium intake is effective in inhibiting neointima formation in vivo.

Animals↗
PubMed1997

Resistance to insecticides in insect vectors of disease: est alpha 3, a novel amplified esterase associated with amplified est beta 1 from insecticide resistant strains of the mosquito Culex quinquesfasciatus.

Vector control programmes in many countries face the dual problems of parasite drug resistance and insecticide resistance in the insect vectors of the disease. Here we report for the first time a new esterase-based insecticide resistance mechanism in the filariasis vector Culex quinquefasciatus. The field collected COL strain of C. quinquefasciatus from Columbia was heterogeneous for organophosphorus insecticide resistance. On native polyacrylamide gels it had an elevated beta-naphthyl acetate specific esterase with the same Rf as that for the Est beta 1s involved in insecticide resistance in other strains of this mosquito species. After five generations of temephos insecticide selection, both the esterase specific activity with p-nitrophenyl acetate and the temephos LC50 values were increased, suggesting that elevation of esterase activity was the underlying mechanism of resistance. Western blots with antisera raised to Est alpha 2(1) and Est beta 2(1) from C. quinquefasciatus indicated that the COL strain had an elevated Est alpha 3 enzyme which co-migrated on native gels with Est beta 1. Southern blots indicated that an est alpha 3 gene was amplified in the COL strain and a Cuban mosquito strain (MRes), although the restriction digest patterns of the est beta 1 genes in these two strains are different. In contrast, the Californian TEMR strain, with the amplified est beta 1(1) gene, had no associated elevated Est alpha. Restriction digest patterns for COL and TEMR DNA suggest that they contain an identical est beta 1(1) gene, but our data suggest that the est alpha 3 gene occurs on the same amplicon as an est beta 1 gene although the genes are probably > 10 kb apart. Hence, either the COL strain has two est beta 1 genes or the est beta 1(1) amplicon in TEMR has been disrupted at some stage during the long colonisation of this strain and the amplified est alpha has been lost.

Animals↗
PubMed2006

Vascular endothelial growth factor-regulated ovarian cancer invasion and migration involves expression and activation of matrix metalloproteinases.

Vascular endothelial growth factor (VEGF) expression is elevated in primary ovarian tumors and metastases. We examined the effect of VEGF on epithelial ovarian cancer (EOC) in vitro invasion and migration and underlying mechanisms. Using the Matrigel invasion assay and colloidal gold phagokinetic track assay, we found that VEGF induced EOC DOV13 invasion and migration in a matrix metalloproteinase (MMP)-dependent manner. Using Western blotting, we show that VEGF, at 20-80 ng/ml, induced secretion of pro-MMP-7 and pro-MMP-9 and activation of pro-MMP-2 in DOV13 conditioned medium in a concentration-dependent manner. However, gelatinolytic activity and total MMP-7 protein in DOV13 conditioned medium reached the maximum upon VEGF treatment at 20-40 ng/ml and decreased at higher-concentration VEGF treatment (80 ng/ml), as shown by DQ-gelatin degradation assay and ELISA. In addition to the effect on MMP secretion/activation, VEGF stimulated secretion of TIMP-2; and blocking TIMP-2 activity by an anti-TIMP-2 MAb significantly increased VEGF (80 ng/ml)-induced DOV13 invasion (p < 0.05), suggesting that VEGF may regulate MMP-2 activity in DOV13 conditioned medium through TIMP-2. Using real-time PCR, we found that VEGF, at 20 ng/ml, significantly increased the expression of VEGFR-1 and VEGFR-2 by approximately 4-fold and 31-fold, respectively, compared to untreated control (p < 0.05). However, the inducing effect of VEGF on VEGFR-2 expression and the internal expression of VEGF121 in DOV13 cells decreased with increasing of VEGF concentration, suggesting the existence of a negative feedback regulatory mechanism. In summary, our results indicate that VEGF may regulate EOC invasion and migration through VEGFR-mediated secretion and activation of MMPs.

Blotting, Western↗
PubMed2002

Increased neutrophil migratory activity after major trauma: a factor in the etiology of acute respiratory distress syndrome?

OBJECTIVE: Neutrophil infiltration of the lung is characteristic of early posttraumatic acute respiratory distress syndrome (ARDS). This study examines the ability of neutrophils isolated (over the first 24 hrs) from the peripheral blood of patients admitted after major trauma to migrate in response to interleukin-8. Interleukin-8 is elevated in the lung within 2 hrs of major trauma in patients who later develop ARDS, and thus it plays a central role in the recruitment of neutrophils to the lung and their subsequent activation. We hypothesized that enhanced interleukin-8-mediated neutrophil migratory activity in the early postinjury phase, before the development of ARDS, may be a crucial factor in the etiology of ARDS. DESIGN: Prospective observational study. SETTING: University Hospital Wales, the Royal Gwent Hospital, and East Glamorgan General Hospital. Laboratory work was conducted at the Institute of Nephrology. PATIENTS: Adult blunt trauma victims with Injury Severity Score > or = 18. MEASUREMENTS AND MAIN RESULTS: Neutrophils were isolated from citrated blood from 17 adult blunt major trauma patients at admission (0 hrs) and 8 and 24 hrs later. Identical samples were obtained from normal laboratory volunteers (n = 9). The neutrophil count in each specimen was measured, and the number of neutrophils migrating across porous tissue culture inserts in response to defined concentrations of interleukin-8 (0, 10, 30, and 100 ng/mL) was quantitated by peroxidase assay. Neutrophil counts in the whole blood specimens obtained from those later developing ARDS were elevated significantly at admission and declined rapidly throughout the next 24 hrs. Significantly greater numbers of trauma patients' neutrophils migrated to concentrations of interleukin-8 (30 and 100 ng/mL) at each time point when compared with normal volunteers (Mann-Whitney U test, p <.05). Neutrophils isolated from major trauma patients exhibited an enhanced migratory response to high concentrations of interleukin-8 throughout the first 24 hrs of admission, in contrast to the normal physiologic attenuation of migration seen in neutrophils isolated from normal laboratory volunteers. CONCLUSIONS: These data indicate that major blunt trauma enhances the migratory capacity of circulating neutrophils. This is manifest within 2 hrs of admission and may be attributable to alteration in interleukin-8 receptor expression, affinity, or downstream signaling. In patients who later develop ARDS, initially elevated circulating neutrophil counts decrease rapidly, over the same time course. Early enhanced neutrophil migratory activity coupled with elevated pulmonary concentrations of interleukin-8 may be central to the establishment of the neutrophil infiltration that is characteristic of ARDS.

Acute Disease↗
PubMed2003

Using stable and radioactive isotopes to trace atmospherically deposited Pb in montane forest soils.

Atmospheric deposition of lead (Pb) throughout the 1900s resulted in elevated amounts of this toxic metal even in remote forest soils of the northeastern United States. Soils can act as a net sink for metals and thus minimize groundwater and surface water contamination. Recent studies utilizing forest floor temporal data and models of total Pb in precipitation, surface soils, and streams have estimated the time scale of Pb release from soils. However, due to the limited availability and spatial variability of forest floor survey data, other methods for quantifying anthropogenic Pb movement are needed. This study uses the isotopic composition (206Pb/207Pb) of soil Pb and measurements of 210Pb and 226Ra to directly trace the transit of atmospherically deposited Pb in the soil profile. We also report on the recovery of an enriched 207Pb dose applied in 1984 to the surface of a soil plot in the coniferous forest at Camels Hump in Vermont. The isotopic composition of soil Pb in low elevation deciduous forests suggests that approximately 65% of the original atmospheric Pb load has migrated from the forest floor to the upper 10 cm of the mineral soil. Higher elevation sites with coniferous vegetation have thicker forest floors, which have prevented significant amounts of Pb from entering the mineral soil. After 17 years, the soil organic horizon in the coniferous zone prevented any penetration of the applied Pb into the mineral soil. Using 210Pb budgets in different soil compartments, we determine forest floor response times for atmospherically delivered Pb to be approximately 60 years in the low elevation deciduous forest zone and 150 years for the high elevation spruce-fir forest zone at Camels Hump. According to its distribution in the soil profile, we conclude that a dispersed release of anthropogenic Pb to groundwater and surface water is possible this century. Our results also offer independent confirmation of Pb deposition models previously generated for the region.

Air Pollutants↗
PubMed2001

Elevated potassium intake inhibits neointimal proliferation in the swine coronary artery.

BACKGROUND: Previously, we reported that elevated extracellular potassium concentration in vitro inhibited proliferation and migration of vascular smooth muscle cells, formation of free radical compounds by macrophages, and reduced platelet sensitivity to agonists. More recently, we described a reduction in neointimal proliferation after balloon angioplasty injury in the carotid arteries of rats associated with an elevation of dietary potassium intake during a 4-week experiment. In the present study we conducted a similar investigation in the swine coronary artery balloon angioplasty model. PROCEDURES: Two groups of seven castrated male swine were studied; for 28 days the normal potassium group consumed a diet containing 0.25% potassium and the high potassium group ate diet containing 2.0% potassium. After 14 days on the diet, balloon angioplasty was performed. After an additional 14 days on the same diets the hearts were removed, and normal and lesioned sections of the artery were analyzed histologically. RESULTS: The neointimal area was markedly less in the high potassium group than in the normal potassium group, 0.33+/-0.04 mm2 v 0.74+/-0.10 mm2 (P < .004). Neointimal area-to-total wall area ratio in the normal potassium group averaged 0.199+/-0.018, significantly greater than the ratio computed for the elevated potassium group, 0.120+/-0.015 (P < .006). CONCLUSION: These results support the hypothesis that a high level of dietary potassium intake inhibits neointimal proliferation after balloon angioplasty in the swine coronary artery.

Aldosterone↗