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PubMed1998

Effects of intensive endurance exercise on DNA damage in leucocytes.

OBJECTIVE: It has been shown that highly intensive anaerobic exercise induces DNA damage in leucocytes (LEU). The present study was designed to investigate whether intensive endurance exercise is capable of inducing comparable effects. EXPERIMENTAL DESIGN: A prospective study. PARTICIPANTS: Twelve men (aged 27.3 +/- 4.1 years) who undertook a regular training of different extent (running volume 45 +/- 25 km.week-1) volunteered in the study. INTERVENTIONS: The subjects competed in a half marathon (HM) of 21.1 km, 93.0 +/- 10.4 min. MEASUREMENTS: Blood was taken at rest, 1 and 24 hrs after HM for determination of creatine kinase, neutrophil (PMN), lymphocyte and monocyte counts. DNA damage in LEU at rest and 24 hrs after HM was quantified using the single cell gel-electrophoresis (SCG) assay. RESULTS: PMN increased from 2.81 +/- 0.69 to 13.13 +/- 2.91 1 hrs after HM (p < 0.01) and returned to 3.26 +/- 0.47 10(9) cells.l-1 by 24 hr recovery. DNA migration (image length, IL) reflecting the extent of DNA damage was elevated significantly in 10 of 12 subjects one day after HM. IL rose from 32.7 +/- 2.2 to 40.7 +/- 3.9 microns (p < 0.01). Correlation analysis revealed a relationship between DNA migration 24 hrs after HM and PMN count 1 hr post-exercise (r = 0.67, p < 0.05). CONCLUSIONS: The results confirm the hypothesis that DNA damage in LEU occurs after intensive endurance exercise. We suppose our observation of exercise-induced DNA damage in LEU is affected by reactive oxygen species which are released from PMN. It is quite unclear whether DNA damage in LEU is causal involved in exercise-induced modifications of the immune system.

Adult↗
PubMed2005

Angiotensin II receptor inhibition prevents pneumocyte apoptosis in surfactant-depleted rat lungs.

Pneumocyte apoptosis is implicated in the pathophysiology of acute inflammatory lung injuries in newborns and adults. Pulmonary angiotensin (ANG) II contributes to lung epithelial apoptosis in vitro, but its role in acute lung injury in vivo is unclear. We therefore studied the effects of ANG II receptor action on the pulmonary inflammatory and apoptotic changes in surfactant-depleted lungs in rats. Lung injury was induced by repeated lung lavage with saline, and the rats were then ventilated with 60% oxygen for 1, 3, or 5 hr. Separate groups of rats were pretreated with a nonspecific ANG II receptor inhibitor saralasin, the specific ANG II type 1 receptor antagonist losartan, or ANG II type 2 receptor inhibitor PD123319, and were similarly studied. Lungs were studied histologically for tissue injury, and with terminal deoxynucleodityl transferase-mediated dUTP nick end-labeling (TUNEL) and cleaved caspase 3 antibody staining, and by electron microscopy for apoptotic cell death. Surfactant-depleted lungs showed an increased number of TUNEL-positive epithelial cells throughout the study, and intrapulmonary leukocyte migration and histological tissue injury scores were similarly elevated, compared to controls, from 1-5 hr of ventilation. Pretreatment with saralasin or losartan significantly prevented the increase of TUNEL positivity in pneumocytes, but had no effect on the amount of neutrophil influx or total injury score in lavaged lungs. In contrast, administration of PD123319 did not affect the number of TUNEL-positive epithelial cells or histological injury . The results suggest that increased epithelial apoptosis in surfactant-deficient lungs is mediated by ANG II receptor (specifically, subtype 1) action.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2002

Inadvertent intrathecal use of ionic contrast agent.

Intrathecal administration of ionic contrast media may cause severe and fatal neurotoxic reactions due to their hyperosmolarity and ionic nature. They are therefore strictly contraindicated for all radiologic applications involving the central nervous system (e.g., myelography). We present a case in which ioxitalamate was accidentally injected intrathecally. The patient recovered completely due to a combination of the different therapeutic options reported in the literature, including early mechanical ventilation and neuromuscular paralysis, aggressive control of seizures, elevation of head and trunk to prevent cephalad migration of contrast, steroids, cerebrospinal fluid drainage and lavage and prophylactic antibiotics.

Contrast Media↗
PubMed2004

Height changes associated with pigment aggregation in Xenopus laevis melanophores.

Melanophores are pigment cells found in the skin of lower vertebrates. The brownish-black pigment melanin is stored in organelles called melanosomes. In response to different stimuli, the cells can redistribute the melanosomes, and thereby change colour. During melanosome aggregation, a height increase has been observed in fish and frog melanophores across the cell centre. The mechanism by which the cell increases its height is unknown. Changes in cell shape can alter the electrical properties of the cell, and thereby be detected in impedance measurements. We have in earlier studies of Xenopus laevis melanophores shown that pigment aggregation can be revealed as impedance changes, and therefore we were interested in investigating the height changes associated with pigment aggregation further. Accordingly, we quantified the changes in cell height by performing vertical sectioning with confocal microscopy. In analogy with theories explaining the leading edge of migrating cells, we investigated the possibility that the elevation of plasma membrane is caused by local swelling due to influx of water through HgCl2-sensitive aquaporins. We also measured the height of the microtubule structures to assess whether they are involved in the height increase. Our results show that pigment aggregation in X. laevis melanophores resulted in a significant height increase, which was substantially larger when aggregation was induced by latrunculin than with melatonin. Moreover, the elevation of the plasma membrane did not correlate with influx of water through aquaporins or formation of new microtubules, Rather, the accumulation of granules seemed to drive the change in cell height.

Animals↗
PubMed1990

Seasonal changes in serum gonadal steroids associated with migration, mating, and nesting in the loggerhead sea turtle (Caretta caretta).

Adult male loggerhead sea turtles, Caretta caretta, exhibited a "prenuptial" spermatogenic cycle that was coincident with increased concentrations of serum testosterone (T). Serum T was high during the months when migration and mating have been recorded for males. In contrast to females, males appear to be annual breeders. Nine reproductively active female C. caretta (as verified through laparoscopy) were tagged with sonic transmitters and were repeatedly bled prior to migration. Four months prior to the nesting season, the ovaries of reproductively active females had hundreds of vitellogenic follicles of approximately 1.5 cm in diameter (i.e., half the size of ovulatory follicles). Approximately 4-6 weeks prior to migration from feeding grounds to mating and nesting areas, serum estradiol-17 beta (E2) concentrations increased significantly and remained high for approximately 4 weeks, suggesting a period of increased vitellogenesis. During a 1- to 2-week period prior to migration, serum E2 decreased significantly, while serum T concentrations increased (at least) until the time of migration. Serum T, E2, and progesterone (PRO) were elevated during nesting if a turtle was going to nest again during that nesting season. During the last nesting of a season, turtles had low serum concentrations of T, E2, and Pro. The prenuptial pattern of gonadal recrudescence and gonadal steroid production in both male and female C. caretta contrasts with those of many temperate freshwater turtles, and this type of reproductive pattern may have been facilitated by adaptation to a tropical marine environment.

Animals↗
PubMed1994

Effect of TFC-612, a 7-thia prostaglandin E1 derivative, on intimal thickening after endothelial injury with balloon catheter in rats.

The effect of TFC-612, methyl-6-[(1R,2S,3R)-hydroxy-2-](1E,3S,5R)-3- hydroxy-5-methyl-1-nonenyl]-5-oxocyclopentyl)thio] hexanoate, on intimal thickening of carotid artery 14 days after endothelium denudation with a balloon catheter was examined in rats. This compound significantly suppressed the neointimal area and the ratio of intimal and medial layer by 41.1% and 31.4%, respectively, at 3.2 micrograms/rat/h s.c. infusion. At this dose, this compound did not inhibit platelet aggregation induced by either collagen or ADP. It did not inhibit bromodeoxyuridine incorporation into medial smooth muscle cells at 3 days after injury. In in vitro experiments, TFC-612 did not inhibit the [3H]thymidine uptake into cultured smooth muscle cells, but it showed significant inhibition of smooth muscle cell migration induced by platelet-derived growth factor (PDGF) at more than 10(-9) M. This compound increased cyclic AMP levels dose dependently in cultured smooth muscle cells at more than 10(-8) M. These results suggest that TFC-612 inhibits intimal thickening by inhibition of smooth muscle cell migration from media to intima through cyclic AMP elevation.

Alprostadil↗
PubMed1975

Appearance of acetylcholinesterase and creatine kinase in plasma of normal chickens after denervation.

Evidence that acetylcholinesterase (AChE) activity is released from normal chick embryonic muscle fibers and from muscles of chickens with inherited muscular dystrophy suggested that denervated chick muscles, which have AChE properties similar to dystrophic muscles, would also release AChE. Bilateral denervation of the breast and wing muscles of normal chickens was followed by the appearance of AChE activity, distinguished from plasma cholinesterase by differential substrate hydrolysis, inhibitor sensitivity, and electrophoretic migration. Plasma creatine kinase (CK) activity was also elevated after denervation.

Acetylcholinesterase↗
PubMed1996

Selecting valid in vitro biocompatibility tests that predict the in vivo healing response of synthetic vascular prostheses.

We have investigated the usefulness of six in vitro biocompatibility tests in predicting the healing performance of polyester vascular prostheses as observed in previous canine in vivo trials. Vascular grafts were evaluated by using (i) a direct contact (DC) assay, (ii) an extract dilution (ED) assay on murine fibroblast cells, (iii) a DC assay on endothelial cells, (iv) a complement activation study, (v) a leucocyte activation study of CD18 integrin subunit expression on human polymorphonuclear cells (PMNs) and (vi) interleukin-2 receptor expression on lymphocytes. Uncleaned polyester grafts had previously been associated with poor healing and gelatin-impregnated polyester grafts with delayed but satisfactory healing, whereas commercially cleaned polyester grafts had demonstrated excellent healing. Lightweight and heavyweight knitted and woven polyester grafts supplied specifically for this project were studied, each with a different surface condition, i.e. commercially available (CP), uncleaned (UP) and impregnated with gelatin (GP). The UP grafts induced fibroblast cytotoxicity according to the ED assay, poor migration and viability of endothelial cells, and an elevated expression of CD18 and interleukin-2 receptor on PMNs and lymphocytes, respectively. In contrast, the CP grafts promoted good endothelial cell growth, no evidence of cytotoxicity and a weaker cell activation, and the GP grafts were found to be non-cytotoxic, to exhibit a good cellular response and to moderate cell activation. The complement activation assay and the DC assay on fibroblasts were found to be less useful and less discriminating. From this, it is concluded that the two cell activation measurements, the DC assay on endothelial cells and ED assay on fibroblasts, are useful in predicting the in vivo healing response of arterial polyester substitutes.

Analysis of Variance↗
PubMed1986

A practical score for the early diagnosis of acute appendicitis.

We conducted a retrospective study of 305 patients hospitalized with abdominal pain suggestive of acute appendicitis. Signs, symptoms, and laboratory findings were analyzed for specificity, sensitivity, predictive value, and joint probability. The total joint probability, the sum of a true-positive and a true-negative result, was chosen as a diagnostic weight indicative of the accuracy of the test. Eight predictive factors were found to be useful in making the diagnosis of acute appendicitis. Their importance, according to their diagnostic weight, was determined as follows: localized tenderness in the right lower quadrant, leukocytosis, migration of pain, shift to the left, temperature elevation, nausea-vomiting, anorexia-acetone, and direct rebound pain. Based on this weight, we devised a practical diagnostic score that may help in interpreting the confusing picture of acute appendicitis.

Acute Disease↗
PubMed1992

A small (58-nm) attached sphere perturbs the sieving of 40-80-kilobase DNA in 0.2-2.5% agarose gels: analysis of bacteriophage T7 capsid-DNA complexes by use of pulsed field electrophoresis.

Although the icosahedral bacteriophage T7 capsid has a diameter (58 nm) that is 234-fold smaller than the length of the linear, double-stranded T7 DNA, binding of a T7 capsid to T7 DNA is found here to have dramatic effects on the migration of the DNA during both pulsed field agarose gel electrophoresis (PFGE; the field inversion mode is used) and constant field agarose gel electrophoresis (CFGE). For these studies, capsid-DNA complexes were obtained by expelling DNA from mature bacteriophage T7; this procedure yields DNA with capsids bound at a variable position on the DNA. When subjected to CFGE at 2-6 V/cm in 0.20-2.5% agarose gels, capsid-DNA complexes arrest at the electrophoretic origin. Progressively lowering the electrical potential gradient to 0.5 V/cm results in migration; most complexes form a single band. The elevated electrical potential gradient (3 V/cm) induced arrest of capsid-DNA complexes is reversed when PFGE is used instead of CFGE. For some conditions of PFGE, the mobility of capsid-DNA complexes is a function of the position of the capsid on the DNA. During either CFGE (0.5 V/cm) or PFGE, capsid-DNA complexes increasingly separate from capsid-free DNA as the percentage of agarose increases. During these studies, capsid-DNA complexes are identified by electron microscopy of enzymatically-digested pieces of agarose gel; this is apparently the first successful electron microscopy of DNA from an agarose gel.(ABSTRACT TRUNCATED AT 250 WORDS)

Capsid↗
PubMed2003

Thermodynamic rearrangement synthesis and NMR structures of C1, C3, and T isomers of C60H36.

The structures of three C60H36 isomers, produced by high-temperature transfer hydrogenation of C(60) in a 9,10-dihydroanthracene melt, was accomplished by 2D (1)H-detected NMR experiments, recorded at 800 MHz. The unsymmetrical C(1) isomer is found to be the most abundant one (60-70%), followed by the C(3) isomer (25-30%) and the least abundant T isomer (2-5%). All three isomers are closely related in structure and have three vicinal hydrogens located on each of the 12 pentagons. Facile hydrogen migration on the fullerene surface during annealing at elevated temperatures is believed to be responsible for the preferential formation of these thermodynamically most stable C60H36 isomers. This hypothesis was further supported by thermal conversion of C60H36 isomers to a single C(3v) isomer of C60H18.

Journal Article↗
PubMed1998

Antigen direction of specific T-cell clones into gingival tissues.

This study was performed to investigate T-cell traffic to periodontal tissues during infection with a periodontal pathogen Actinobacillus actinomycetemcomitans (Aa). Rowett rat T-cell clones, A3 (CD4+ CD8-, alpha beta TCR+, NKRP-1-, specific to Aa) and G2 (CD4- CD8-, alpha beta TCR+, NKRP-1+, which reacts to Aa, Gram-negative and -positive bacteria), both expressed the same prominent adhesion molecules (LFA-1, VLA-4) to the same extent. Binding of both T-cell clones to rat endothelial cells in vitro was blocked by antibody to VLA-4. Rowett rats were infected with Aa and infused with Aa-stimulated, isogenic T-clone lymphocytes that had been labelled in vitro with 125IUdR. Radioactivity associated with recovery of clone A3, but not G2, was significantly elevated in the gingivae of infected rats, suggesting migration to infected animals' gingival tissues. Migration of radioactive Aa-specific A3 clone cells traced by autoradiography reached a maximum at 24 hr (1.2% of total lymphocytes as radiolabelled cells in infected gingiva versus 0.6% in noninfected), indicating an apparent antigen-directed retention in infected rats' gingival tissues. The G2 clone was not retained in the gingival tissues (0.20% of total lymphocytes as radiolabelled cells in infected gingiva versus 0.26% in non-infected). However, the possibility of A3 retention directed by inflammation or tissue-selective homing could not be excluded. In further experiments, other adoptively transferred T-clone lymphocytes [clones G23 (Th1) and F13 (Th2)] with specificity for the 29,000 MW outer membrane protein of Aa with the same prominent adhesion molecules could be recovered from rat gingivae previously challenged with this antigen. However, transferred T-clone lymphocytes [clone G26 (Th1)] with specificity for a different Aa antigen were not recovered. Therefore, the dynamics of cell entry into periodontal lesions vary for activated T lymphocytes with different antigenic specificities, indicating the significance of antigen in lymphocyte traffic to periodontal tissues.

Actinobacillus Infections↗
PubMed2000

Neurotrophin-3 controls proliferation of granular precursors as well as survival of mature granule neurons in the developing rat cerebellum.

Levels of neurotrophin-3 markedly decrease in the rat cerebellum after the first 10 days of life, suggesting an importance during early development. To further examine the effect of neurotrophin-3 on the developing cerebellum, we injected a monoclonal antibody against neurotrophin-3 into the lateral ventricle of 7.5-day-old rats. The resultant depletion of neurotrophin-3 caused a significant decrease in cerebellar wet weights noted at 7 and 23 days thereafter. Other changes noted 48 h after injection of monoclonal antibodies against neurotrophin-3 included reduced incorporation of bromode-oxyuridine into granule neurons in the external germinal layer, an elevated density of atrophic neurons that had just migrated under the Purkinje cell layer, and an increased number of apoptotic neurons in the internal granule cell layer. These changes were limited to the central lobe. The concentration of neurotrophin-3 protein in the posterior region, including the central lobe, was about four- and threefold higher than that in the anterior region of the cerebellum of 9.5- and 30-day-old rats, respectively. Immunocytochemical examination showed higher amounts of neurotrophin-3 protein in the central lobe than in the anterior lobe. Our results provide evidence that neurotrophin-3 regulates the proliferation of granule precursors and supports the survival of mature granule neurons in restricted lobules, suggesting an involvement in limited regions at a specific stage in development of the rat cerebellum.

Aging↗
PubMed2001

Humoral markers of severity and prognosis of critical illness.

Despite the considerable advances made in understanding the pathophysiology of systemic inflammation during critical illness, clinical progress has been elusive as it remains a very deadly condition. Cortisol and thyroid hormone levels can be as predictive of outcome as the commonly used severity parameters (i.e. APACHE). Indeed, levels of endocrine humoral substances such as arachidonic acids, nitric oxide, endothelin, calcitonin precursors, leptin and adenosine correlate with the severity and outcome of critical illness. Furthermore, calcitonin precursors represent a potentially new hormokine paradigm, being transcriptionally activated in all cells in response to infection. The cytokines are immune markers that often correlate with severity and outcome, but their release is transient. In contrast, the so-called acute phase proteins, such as C-reactive protein and serum amyloid A, are highly sensitive to inflammatory activity and can be important markers of severity and outcome. Leukocyte esterase, adhesion molecules, platelet activating factor and activated protein C are additional humoral immune markers; the replacement of the latter has been shown to be a promising therapeutic option. Natriuretic peptides are neurocrine humoral markers that have important cardiovascular implications. The level of macrophage migrating inhibitory factor, released by the pituitary, is elevated in sepsis and counteracts glucocorticoid action. Cellular markers to severe stress include the enhanced expression of protective substances in the form of heat shock proteins. High mobility group-1 is a DNA-binding protein and a late mediator of the inflammatory response. Apoptotic markers such as the soluble fas ligand are also elevated in inflammation. In summary, during critical illness, the endocrine, immune and nervous systems elaborate a multitude of humoral markers, the roles of which merit further scrutiny in order to improve therapeutic outcome.

Animals↗
PubMed2000

p120 catenin regulates the actin cytoskeleton via Rho family GTPases.

Cadherins are calcium-dependent adhesion molecules responsible for the establishment of tight cell-cell contacts. p120 catenin (p120ctn) binds to the cytoplasmic domain of cadherins in the juxtamembrane region, which has been implicated in regulating cell motility. It has previously been shown that overexpression of p120ctn induces a dendritic morphology in fibroblasts (Reynolds, A.B. , J. Daniel, Y. Mo, J. Wu, and Z. Zhang. 1996. Exp. Cell Res. 225:328-337.). We show here that this phenotype is suppressed by coexpression of cadherin constructs that contain the juxtamembrane region, but not by constructs lacking this domain. Overexpression of p120ctn disrupts stress fibers and focal adhesions and results in a decrease in RhoA activity. The p120ctn-induced phenotype is blocked by dominant negative Cdc42 and Rac1 and by constitutively active Rho-kinase, but is enhanced by dominant negative RhoA. p120ctn overexpression increased the activity of endogenous Cdc42 and Rac1. Exploring how p120ctn may regulate Rho family GTPases, we find that p120ctn binds the Rho family exchange factor Vav2. The behavior of p120ctn suggests that it is a vehicle for cross-talk between cell-cell junctions and the motile machinery of cells. We propose a model in which p120ctn can shuttle between a cadherin-bound state and a cytoplasmic pool in which it can interact with regulators of Rho family GTPases. Factors that perturb cell-cell junctions, such that the cytoplasmic pool of p120ctn is increased, are predicted to decrease RhoA activity but to elevate active Rac1 and Cdc42, thereby promoting cell migration.

Actins↗
PubMed2004

Functional analysis of cytoplasmic dynein heavy chain in Caenorhabditis elegans with fast-acting temperature-sensitive mutations.

Cytoplasmic dynein, a minus-end-directed microtubule motor, has been implicated in many cellular and developmental processes. Identification of specific cellular processes that rely directly on dynein would be facilitated by a means to induce specific and rapid inhibition of its function. We have identified conditional variants of a Caenorhabditis elegans dynein heavy chain (DHC-1) that lose function within a minute of a modest temperature upshift. Mutant embryos generated at elevated temperature show defects in centrosome separation, pronuclear migration, rotation of the centrosome/nucleus complex, bipolar spindle assembly, anaphase chromosome segregation, and cytokinesis. Our analyses of mutant embryos generated at permissive temperature and then upshifted quickly just before events of interest indicate that DHC-1 is required specifically for rotation of the centrosome/nucleus complex, for chromosome congression to a well ordered metaphase plate, and for timely initiation of anaphase. Our results do not support the view that DHC-1 is required for anaphase B separation of spindle poles and chromosomes. A P-loop mutation identified in two independent dominant temperature-sensitive alleles of dhc-1, when engineered into the DHC1 gene of Saccharomyces cerevisiae, conferred a dominant temperature-sensitive dynein loss-of-function phenotype. This suggests that temperature-sensitive mutations can be created for time-resolved function analyses of dyneins and perhaps other P-loop proteins in a variety of model systems.

Alleles↗
PubMed1989

Differential susceptibility of a fish, tilapia Oreochromis mossambicus (Teleostei, Cichlidae) to hepatocarcinogenesis by diethylnitrosamine and methylazoxymethanol acetate.

Oreochromis mossambicus, commonly known as tilapia, is a freshwater teleost with a wide tolerance to environmental conditions. Multiple focal lesions in the liver were observed 2 months after cessation of a one-month long treatment with 100 p.p.m. diethylnitrosamine. Cells were small and compact and arranged in sheets. Ultrastructurally, these cells have abundant endoplasmic reticulum, round mitochondria, less conspicuous golgi apparatus and fat droplets. Other organs like the intestines, spleen, kidneys, ovaries and pituitary appeared normal. Two liver inducible enzymes, gamma-glutamyl transferase and tyrosine aminotransferase were elevated by 5- and 3-fold respectively. Aggressive migration of hepatocytes was observed in tumorigenic liver explants. Vitellogenesis and early embryological development appeared unaffected as the female fish spawned during hepatocarcinogenesis. However, their fry were stunted and short-lived. To compare the susceptibility of tilapia to another hepatocarcinogen, the fish were also treated with methylazoxymethanol acetate at 10 p.p.m. for 0.5-1 h. However, methylazoxymethanol acetate was too toxic and 75% of the fish succumbed 1 day after treatment. Moreover, after 2 months post-treatment, neither tumors nor change in enzyme activities were observed in any organ. These results suggest that tilapia could be a useful model for screening and differentiating carcinogens since they could develop liver tumors within only 2 months after treatment with diethylnitrosamine.

Animals↗
PubMedDate not supplied

Thalamic ablations and neocortical development: alterations of cortical cytoarchitecture and cell number.

The diversity of neocortical cytoarchitecture could arise from genetic prespecification of cell types and numbers in the ventricular zone, by interaction of cells with their immediate environment, efferent targets, or afferent inputs. Here, we examine the role of the thalamus as efferent target or afferent source in the early control of cell number and type in the developing neocortex. Electrolytic lesions of the thalamus were made in hamsters at birth prior to the thalamic innervation of layer IV. By postnatal day 7, when migration to the cortex is complete, there were no differences in cell number between the cortical plate contralateral and ipsilateral to the thalamic lesion, showing that the absence of thalamic input does not influence the last phases of neocortical cell generation or migration. However, the incidence of pyknotic cells was elevated in the upper half of the cortical plate at this time. By adulthood, the number of cells per unit column of cortex was reduced, due to the apparent absence of small, nonpyramidal cells of layer IV, as determined from Nissl-stained material. Therefore, some of the cytoarchitectonic variability of the neocortex could arise epigenetically by the interaction of neocortical cells with their afferent connections.

Animals↗