Search

We studied life history and secondary production of a caddisfly scraper, Glossosoma nigrior, in two Alabama streams. Collier Creek, located within the Appalachian Plateau physiographic province, is underlain by sandstone bedrock, while Hendrick Mill Branch is located in the Valley and Ridge physiographic province with limestone bedrock. G. nigrior populations in both streams exhibited trivoltine life histories, which were attributed to the higher water temperature regimes than those found in more northern streams. Mean larval density (556 m−2) and biomass (B) (49.2 mg AFDM m−2) were much higher in Hendrick Mill Branch than Collier Creek (78 m−2 and 6.7 mg AFDM m−2). G. nigrior in Hendrick Mill Branch maintained continuous larval growth and higher larval density than Collier Creek throughout the year mainly due to a greater availability of optimal habitat, a more stable hydrology, and warmer winter water temperature. These factors also resulted in the much higher annual secondary production (P) in Hendrick Mill Branch (965 mg AFDM m−2; P/B = 18.3) than Collier Creek (115 mg AFDM m−2; P/B = 17.9). Gut content analysis revealed that algae (>50%) and detritus (>40%) were the major diet items for G. nigrior, and the majority of secondary production (>80%) was contributed by the consumption of algae. Glossosoma populations play an important role in trophic linkage in these streams with their high production and grazing activities.

Polytetrafluoroethylene (PTFE) arteriovenous (AV) grafts are performed routinely for vascular access. The limited life span of PTFE grafts is a major cause of morbidity. Graft failure is attributed to venous outflow tract vascular smooth muscle (VSM) hyperplasia, which is linked to heterotrimeric G protein signaling. We proposed that expression of a peptide inhibitor of G(betagamma) signaling (betaARKct) in the venous outflow of PTFE grafts would reduce hyperplasia and prolong graft patency. Left carotid to right external jugular vein PTFE AV grafts were placed in swine. The isolated external jugular vein was treated with an adenovirus encoding betaARKct, empty adenovirus, or phosphate-buffered saline for approximately 25 min. After 7 or 28 days, flow probe analysis was performed and the vein was harvested and analyzed for cross-sectional area comparison. After both 7 and 28 days, when compared to controls, treated animals demonstrated a statistically significant reduction in VSM hyperplasia with a reduction in cross-sectional intimal and medial areas of40% (p0.05). Flow was maintained in treated grafts, while control groups demonstrated a50% reduction (p0.05) at 7 days. Further, treated grafts demonstrated significant improvement in graft patency at 28 days (100% vs. 12% for treated and untreated grafts, respectively). The inhibition of G(betagamma) signaling reduces intimal-medial hyperplasia and prolongs graft patency in PTFE AV grafts. This represents a novel molecular therapeutic strategy for improving the patency of vascular access grafts.

Recent efforts to adapt nitroxide-mediated living radical polymerization chemistry to colloidal systems have shown considerable progress when miniemulsions are used. Miniemulsion SFRP in fact can yield higher conversions (>99%) and faster reaction rates than bulk SFRP. Much of the advantage of operating in miniemulsion arises from the inherent advantages of having a two phase system, in which the aqueous phase can be employed as a medium to introduce rate enhancing additives such as ascorbic acid to the reaction loci with a high degree of control. Additives such as ascorbic acid act by consuming excess nitroxide, and therefore directly influence the rate. Results on the effect of ascorbic addition on rate, molecular weight and livingness are presented. We have also begun to address the issue of high operating temperatures in TEMPO-mediated SFRP (∼120–135 °C) that require a pressurized reactor. We have run experiments using TEMPO at 100 °C with slowly decomposing initiator added to maintain an appropriate free nitroxide concentration. Reasonable reaction rates are obtained, albeit with higher polydispersities (∼1.6). Challenges and opportunities related to lower temperature operation are discussed.

Various physical and biological properties affect solute transport patterns in streams. We measured hydraulic characteristics of Payne Creek, a low-gradient upper Coastal Plain stream, using tracer experiments and parameter estimation with OTIS-P (one-dimensional transport with inflow and storage with parameter optimization). The primary objective of this study was to estimate the effects of varying discharge, season, and litter accumulation on hydraulic parameters. Channel area A ranged from 0·081 to 0·371 m2 and transient storage area As ranged from 0·027 to 0·111 m2. Dispersion D ranged from 1·5 to 11·1 m2 min−1 and exchange coefficient α ranged from 0·009 to 0·038 min−1. Channel area and dispersion were positively correlated to discharge Q, whereas storage area and exchange coefficient were not. Relative storage size As/A ranged from 0·17 to 0·59, and was higher during fall than other seasons under a similar Q. The fraction of median travel time due to transient storage ranged from 8·8 to 34·5% and was significantly correlated with Q through a negative power function. Both metrics indicated that transient storage was a significant component affecting solute transport in Payne Creek, especially during the fall. Comparison between the measured channel area Ac and A suggested that surface storage was dominant in Payne Creek. During fall, accumulation of leaf litter resulted in larger A and As and lower velocity and D than during other seasons with similar discharge. Seasonal changes in discharge and organic matter accumulation, and dynamic channel morphology affected the magnitude of transient storage and overall hydraulic characteristics of Payne Creek. Copyright © 2005 John Wiley & Sons, Ltd.

The 2,2,6,6-tetramethyl-1-piperidinyloxy (TEMPO)-mediated stable free radical polymerization of styrene in miniemulsion at 100 °C is demonstrated. Although this temperature is 20–35 °C lower than typical temperatures used for TEMPO-mediated polymerizations, reasonable reaction rates were achieved by the addition of ascorbic acid or a free radical initiator. More importantly, the living character of the chains was preserved; the degree of polymer “livingness” was comparable to polymerizations conducted at 135 °C. Polydispersities were broader than that observed in well-controlled systems, ranging from ∼1.4–1.6, and consistent with expectations for systems having a low activation rate. The results are significant for two reasons. They will facilitate TEMPO-mediated minemulsion polymerizations in nonpressurized (or minimally pressurized) reactors, and they reveal the potential to expand the traditional temperature range of TEMPO and possibly other nitroxides in bulk, solution, and miniemulsion. © 2005 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 44: 232–242, 2006

Acute and chronic arsenic exposure results in toxicity in humans and causes many neurological and other manifestations. For the first time the present study reports that zinc decreases arsenic-induced apoptosis and also confirms a single report of apoptosis induced by arsenic in a neuronal cell line. Apoptosis measured by DEVD-caspase activity peaked between 10 microM and 20 microM of arsenic trioxide. Higher concentrations of arsenic up to 40 microM caused increasing cell death with diminishing DEVD-caspase activity. The beneficial effect of zinc was proportional to its concentration with a significant decrease in arsenic-induced DEVD-caspase activity at 50 microM and 75 microM zinc (P0.05). This finding may be of therapeutic benefit in people suffering from chronic exposure to arsenic from natural sources, a global problem especially relevant to millions of people on the Indian subcontinent.

Purpose Vascular access polytetrafluoroethylene (PTFE) graft failure is a major cause of morbidity in the hemodialysis population. The most common cause of graft failure is thrombosis secondary to stenosis at the venous outflow tract. Venous outflow stenosis is characterized by intimal-medial hyperplasia. We have developed a porcine arteriovenous (AV) graft model that may be used to investigate this proliferative response and aid in the development of new therapies to prevent intimal-medial hyperplasia and improve graft patency. Methods Left carotid to right external jugular vein PTFE (6 mm) grafts were implanted in the necks of swine. Immediately following anatomosis, flow rates were recorded. In one group of animals (n = 4) the venous outflow tract was harvested after 7 days and morphometric analysis of intimal and medial area was performed. In a second group (n = 8) the graft patency was monitored until 28 days. Results All porcine PTFE fistula grafts were patent at 7 days and 100% patency was maintained until 14 days. After 28 days, 75% of the grafts failed due to thrombosis. The venous outflow tract developed a significant proliferative response. After 7 days the intimal and medial areas were 469 ± 9 μm2 and 875 ± 26 μm2 respectively. At 28 days the intimal and medial areas were 913 ± 55 μm2 and 1437 ± 182 μm2 respectively. Luminal flow rate of the venous outflow tract was reduced significantly (344 ± 11 ml/min at Day 0 to 129 ± 14 ml/min at Day 7, p < 0.05). Conclusions This porcine model rapidly, reliably and robustly reproduces the flow reducing stenosis and intimal-medial hyperplasia at the venous outflow tract of PTFE arteriovenous fistula. It represents a promising tool for investigating the mechanisms of intimal-medial hyperplasia, evaluating therapeutic interventions and new graft materials.

Excessive proliferation of vascular smooth muscle cells (VSMCs) is a critical element in the development of several vascular pathologies, particularly in atherosclerosis and in restenosis due to angioplasty. We have shown that butyrate, a powerful antiproliferative agent, a strong promoter of cell differentiation and an inducer of apoptosis inhibits VSMC proliferation at physiological concentrations with no cytotoxicity. In the present study, we have used cDNA array technology to unravel the molecular basis of the antiproliferative effect of butyrate on VSMCs. To assess the involvement of gene expression in butyrate-inhibited VSMC proliferation, proliferating VSMCs were exposed to 5 mmol/1 butyrate 1 through 5 days after plating. Expression profiles of 1,176 genes representing different functional classes in untreated control and butyrate treated VSMCs were compared. A total of 111 genes exhibiting moderate (2.0–5.0 fold∥ to strong (> 5.0 fold) differential expression were identified. Analysis of these genes indicates that butyrate treatment mainly alters the expression of four different functional classes of genes, which include: 43 genes implicated in cell growth and differentiation, 13 genes related to stress response, 11 genes associated with vascular function and 8 genes normally present in neuronal cells. Examination of differentially expressed cell growth and differentiation related genes indicate that butyrate-inhibited VSMC proliferation appears to involve down-regulation of genes that encode several positive regulators of cell growth and up-regulation of some negative regulators of growth or differentiation inducers. Some of the down-regulated genes include proliferating cell nuclear antigen (PCNA), retinoblastoma susceptibility related protein p130 (pRb), cell division control protein 2 homolog (cdc2), cyclin B1, cell division control protein 20 homolog (p55cdc), high mobility group (HMG) 1 and 2 and several others. Whereas the up-regulated genes include cyclin D1, p21WAF1, p14INK4B/p15INK5B, Clusterin, inhibitor of DNA binding 1 (ID1) and others. On the other hand, butyrate-responsive stress-related genes include some of the members of heat shock protein (HSP), glutathione-s-transferase (GST), and glutathione peroxidase (GSH-PXs) and cytochrome P450 (CYP) families. Additionally, several genes related to vascular and neuronal function are also responsive to butyrate treatment. Although involvement of genes that encode stress response, vascular and neuronal functional proteins in cell proliferation is not clear, cDNA expression array data appear to suggest that they may play a role in the regulation of cell proliferation. However, cDNA expression profiles indicate that butyrate-inhibited VSMC proliferation involves combined action of a proportionally large number of both positive and negative regulators of growth, which ultimately causes growth arrest of VSMCs. Furthermore, these butyrate-induced differential gene expression changes are not only consistent with the antiproliferative effect of butyrate but are also in agreement with the roles that these gene products play in cell proliferation.

Acrolein, a major component of cigarette smoke, an environmental pollutant and an endogenous lipid peroxidation product, has been implicated in the development of atherosclerosis. Although a link between vascular injury and acrolein has been indicated, the exact molecular mechanism of acrolein-induced toxicity to vasculature is unknown. In an effort to elucidate the molecular basis of acrolein-induced vascular toxicity, the possibility of the intracellular signaling system as one of the targets of acrolein-induced toxicity is investigated in the present study. Exposure of cultured rat vascular smooth muscle cells (VSMCs) to different doses of acrolein not only causes cytotoxicity but also alters cellular morphology in a concentration and time-dependent manner. VSMCs exhibit cytotoxicity to a narrow concentration range of 5–10 μg/ml and display no toxicity to 2 μg/ml acrolein even after 24 h of exposure. Furthermore, exposure to acrolein results in activation of members of the mitogen-activated protein kinase (MAPK) family and protein tyrosine kinases. The extracellular signal-regulated kinases 1 and 2 (ERK1/2), stress-activated protein kinases/c-jun NH2-terminal kinases (SAPK/JNK) and p38MAPK are effectively and transiently activated by acrolein in a concentration and time-dependent fashion. While all three MAPKs exhibit significant activation within 5 min of exposure to acrolein, maximum activation (ERK1/2 and p38MAPK) or close to maximum activation (SAPK/JNK) occurs on exposure to 5 μg/ml acrolein for 2 h. Acrolein-induced activation of MAPKs is further substantiated by the activation of transcription factors, c-jun and activator transcription factor-2 (ATF-2), by acrolein-activated SAPK/JNK and p38MAPK, respectively. Additionally several cellular proteins exhibit spectacular protein tyrosine phosphorylation, particularly in response to 2 and 5 μg/ml of acrolein. Interestingly, the acrolein-induced activation of MAPKs precedes acrolein-stimulated protein tyrosine phosphorylation, which occurs after 2 h of exposure to acrolein. However, the time course of maximum protein tyrosine phosphorylation profile corresponds to the peak activation profile of MAPKs. The activation of MAPKs and protein tyrosine phosphorylation by acrolein appears to be independent of acrolein-induced toxicity. VSMCs exposed to 2 μg/ml acrolein exhibit no toxicity but stimulates significant activation of MAPKs and protein tyrosine phosphorylation. Although acrolein-induced VSMC toxicity is not blocked by MAPK inhibitors, PD98059, an inhibitor of MAPK kinase and SB203580, an inhibitor of p38MAPK, either alone or in combination, each MAPK responds differently to the inhibitors. Most prominently, although SB203580, an inhibitor of both SAPK/JNK and p38MAPK, significantly inhibited acrolein-induced activation of p38MAPK, it also stimulated SAPK/JNK activation by acrolein alone and in combination with PD98059. These results provide the first evidence that the activation of both growth-regulated (ERK1/2) and stress-regulated (SAPK/JNK and p38MAPK) MAPKs as well as tyrosine kinases are involved in the mediation of acrolein-induced effects on VSMC, which may play a crucial role in vascular pathogenesis due to environmentally and endogenously produced acrolein.

Epigenetic mechanisms by altering the expression and in turn, functions of target genes, without changing their primary structure have potential to modify cellular processes that are characteristic...

We present morphological data on the four subspecies of painted turtles (Chrysemys picta) from 20 states in the U.S.A. and three provinces in Canada, and from localities within them that are removed from reported zones of intergradation. The characters used are those of Hartman (1958), which have been routinely used in subsequent studies: the extent of plastral patterning (here quantified by image analysis), the degree of misalignment of carapacial scutes, and the width of the light anterior margins of the second lateral scutes. Our purposes are to present descriptive baseline data for each subspecies for use in comparisons with the results of past and future studies of intergradation, and to critique the oft-accepted theory of Bleakney (1958) regarding the evolutionary origins of the current subspecies, particularly C. p. marginata. Data are given for C. p. bellii from 5 states ranging from Minnesota to New Mexico, for C. p. dorsalis from 3 states (Arkansas, Louisiana, and Mississippi), for C. p. marginata from 4 localities (Ontario, Michigan, Indiana, and Ohio), and for C. p. picta from 11 localities from Nova Scotia to Georgia. We find that (i) a "pure" picta does not exist; there is marginata influence throughout picta's range, particularly at the extremes; (ii) similarities exist that group dorsalis with picta; (iii) there is a north-south cline of reduced scute alignment in picta; (iv) there is a north-south cline of increasing extent of the plastral pattern in bellii; (v) the question of which subspecies first reached New England after the Wisconsinan glaciation remains unresolved, but it was likely not picta; (vi) there is no compelling reason to accept or reject Bleakney's theory of the distribution of painted turtle subspecies at the height of the Wisconsinan glaciation or his conjecture that marginata arose as in intergrade of bellii and dorsalis; in fact, it could be argued that if marginata is a hybrid, it could be a hybrid of picta and bellii.

Diarrhoea and constipation are common side effects of many drugs. In older persons, these iatrogenic consequences compound the increased prevalence of acute and chronic illness. An awareness of diarrhoea and constipation as complications of drug therapy in this age group and the use of preventative measures wherever practical may significantly improve the quality of life of the patient. It is important to understand the mechanisms whereby medications may cause diarrhoea and constipation and to periodically review drug use in the elderly. This second part of the review explains the mechanisms of drug-induced constipation and presents examples of drugs commonly associated with this abnormality of bowel function. (author abstract)

Annual flooding in low-gradient rivers is recognized as an important subsidy between the river and its broad adjoining floodplains. Unfortunately, relatively few low- gradient rivers are unregulated and retain their natural "flood pulse" behavior in most developed regions of the world. Furthermore, attempts to quantify flood inundation dy- namics of any river floodplain are scarce. We used aerial photography to delineate the degree of floodplain inundation and GIS to quantify flooded areas on the forested floodplain of a 6.3-km reach of the Ogeechee River, an unregulated sixth-order river in the southeastern USA. A regression was used to quantify the relationship between discharge and percentage floodplain inundation. Using 58 years of daily discharge data obtained from a U.S. Geo- logical Survey gaging station, we converted daily discharge into daily percentage inundation and produced an inundation-duration curve, which describes the percentage of time that a particular inundation level is exceeded. This showed, for example, that >50% of the flood- plain was inundated 15% of the time (54 d/yr) and that 100% was inundated 3.6% of the time (13 d/yr) for the average year. At 50% inundation, system width exceeded channel width by 19 times. In a relatively wet year, we showed that 50-100% of the floodplain was inundated for several months during the winter-spring. Even in a relatively dry year, >20% of the floodplain (seven times the river width) was inundated for several months. The long- term pattern over a period of 58 years (1938-1995) showed considerable fluctuation in inundation and recession occurring throughout most years, with the highest peaks found during winter and spring. The floodplain failed to reach 50% inundation in only four of 58 years. However, in six years, >50% of the floodplain was inundated for at least 30% of the time (i.e., four months of the year). Floods of 50% inundation typically had a duration of at least 30 d. Thus, although inundation may fluctuate considerably within a year, much of the floodplain can be inundated for a relatively long duration. Description of such long- term patterns is essential for understanding natural hydrodynamics of unregulated rivers, particularly as attempts are made to restore previously altered systems. The flood pulse for this forested floodplain river is less predictable and floods are of shorter duration than the large tropical rivers for which the flood pulse concept was originally conceived. Unlike tropical rivers where seasonal patterns of flooding are driven by precipitation, flooding in the Ogeechee River is primarily controlled by seasonal differences in evapotranspiration. Description of inundation dynamics is critical to understanding how plants and animals adapt to a habitat that shifts from dry to lentic to lotic, and in quantifying production of aquatic organisms and ecosystem processes.

Diarrhoea and constipation are common side effects of many drugs. In the elderly, such drug-related iatrogenic conditions compound the increased prevalence of acute and chronic illness. In older persons, an awareness of diarrhoea and constipation as complications of drug therapy and the use of preventative measures wherever practical may significantly increase the quality of life of the patient. It is important to understand the mechanisms whereby medications may cause diarrhoea and constipation and to periodically review drug use in the elderly. The first part of this review explains the mechanisms involved in drug-induced diarrhoea and gives examples of drugs commonly involved. (author abstract)

Arterial injury-induced vascular smooth muscle cell (VSMC) proliferation in intima is the important etiologic factor in vascular proliferative disorders such as atherosclerosis, hypertension and restenosis after balloon angioplasty. Butyrate, a naturally occurring short chain fatty acid, is produced by bacterial fermentation of dietary fiber and by mammary glands of certain mammals. Studies have shown that butyrate at millimolar concentrations, which are physiological, induces growth arrest, differentiation and apoptosis. We examined the effect of physiological concentrations of butyrate on rat VSMC proliferation and proliferation-induced PCNA expression to determine anti-atherogenic potential of butyrate. Butyrate concentrations, closer to physiological range, exhibited antiproliferative effects on both serum-induced proliferation of serum-starved quiescent VSMCs and actively proliferating non-confluent VSMCs. Treatment of serum-starved quiescent VSMCs with 1-8 mmol/l concentration of butyrate caused a concentration-dependent decrease in serum-induced VSMC proliferation and cell proliferation-associated increase in total cellular proteins and RNA levels. Similarly, exposure of actively growing VSMCs to 5 mmol/l butyrate resulted in the inhibition of cell proliferation and proliferation-induced increase in cellular proteins and RNA levels. Furthermore, cellular morphology was significantly altered. Analysis of cell cycle regulatory proteins indicated that levels of PCNA, an excellent marker for cell proliferation, was significantly altered by butyrate both in actively proliferating and serum-induced quiescent VSMCs. These observations suggest that butyrate exhibits potential antiatherogenic capability by inhibiting VSMC proliferation and proliferation-associated increase in PCNA expression and thus merits further investigations regarding therapeutic significance of butyrate in vascular proliferative disorders.

Stroke is a polygenic disorder. Previous genetic studies focused on candidate genes influencing pathogenic processes, with little emphasis on genes influencing vascular risk factors. Previous research linked the ClC-Kb T481S poly- morphism to blood pressure (BP). We therefore undertook an association study to determine the relevance of this poly- morphism to stroke, particularly lacunar stroke, given its strong correlation with hypertension. We genotyped DNA from 180 patients with acute ischaemic stroke (44 having lacunar stroke) and 298 age- and gender-matched controls using a se- quence-specific polymerase chain reaction method (SS-PCR). We found no association between the ClC-Kb T481S poly- morphism and ischaemic stroke (Odds Ratio (OR): 0.87, 95% Confidence Interval (CI): 0.57-1.33). Stratification for stroke subtype did not alter this finding. This polymorphism showed a borderline association with history of hypertension (p=0.06) but was not associated with systolic or diastolic BP (p>0.05). To our knowledge there are no other studies pub- lished on this polymorphism and stroke.

(1998). Use of empirical models of stream invertebrate secondary production as applied to a functional feeding group. SIL Proceedings, 1922-2010: Vol. 26, No. 4, pp. 2024-2029.

Although until recently it is presumed that the greater portion of the genome has no biological role, the current advances in genome research and RNA biology have provided evidence indicating that a large section of the human and most eukaryotic genome is transcribed as nonprotein-coding RNAs or non-coding RNAs (ncRNAs)[1,2]. Only about 2% of the eukaryotic genome sequence codes for protein encoding genes and the remaining so called “junk” DNA are thought to have no functional significance [3, 4]. Based on large scale studies of human and other eukaryotic genomes it is estimated that about 98 % of the transcriptional output of their genomes is RNA that does not encode protein implying that the genomes are gorged with either inept RNA transcripts or with ncRNA transcripts that exhibit unanticipated functions in eukaryotic biology. However, recent development of new technologies in molecular biology and human genetics such as genome tiling [4,5], microarrays, and next generation RNAsequencing (RNA-Seq) [6,7] have enabled the discovery of different types of ncRNAs that do not code for protein product [8-10]. Even though ncRNAs do not encode proteins, they play pivotal roles in the complex networks that are necessary to regulate cellular functions via transcriptional and translational regulation of protein coding genes that are crucial to normal development and physiology, and to disease [11]. Moreover, many of the ncRNAs are highly conserved and susceptible to epigenetic and genetic defects that affect normal development and disease process significantly [12-15].

We studied the relationship between geology and lotic secondary production by analyzing geographical patterns of the distribution, biomass, and production of the freshwater snail Elimia (Pleuroceridae) in Alabama. Nine streams were selected for study, three each in three physiographically distinct regions of uniform climate but contrasting lithology. Our objectives were to assess: 1) the production and biomass of Elimia among streams with contrasting alkalinities due to differences in regional geology--sandstone (5.7 mg/L as CaCo 3 ) 2 , P = 1565 mg/m

Power-law behaviors in brain activity in healthy animals, in the form of neuronal avalanches, potentially benefit the computational activities of the brain, including information storage, transmission and processing. In contrast, power-law behaviors associated with seizures, in the form of epileptic quakes, potentially interfere with the brain's computational activities. This review draws attention to the potential roles played by homeostatic mechanisms and multistable time-delayed recurrent inhibitory loops in the generation of power-law phenomena. Moreover, it is suggested that distinctions between health and disease are scale-dependent. In other words, what is abnormal and defines disease it is not the propagation of neural activity but the propagation of activity in a neural population that is large enough to interfere with the normal activities of the brain. From this point of view, epilepsy is a disease that results from a failure of mechanisms, possibly located in part in the cortex itself or in the deep brain nuclei and brainstem, which truncate or otherwise confine the spatiotemporal scales of these power-law phenomena.

To assess the effect of propofol on the canine sphincter of Oddi (SO), sphincter of Oddi manometry (SOM) was performed in fasting dogs which had undergone cholecystectomy and placement of modified Thomas duodenal cannulae. Using two water-perfused, single-lumen manometric catheters, SO and duodenal pressures were measured simultaneously. Baseline SO activity was recorded for at least one complete interdigestive cycle followed by bolus injections of propofol (Diprivan ®) (N = 31) from 0.1 to 4.0 mg/kg during Phase I of the Migrating Motor Complex (MMC).When propofol was administered in bolus doses ≤ 0.5 mg/kg, no change in SO or duodenal motor function was seen. In doses ≥ 0.5 mg/kg, SO basal pressure, amplitude, and frequency of contractions increased significantly. Increases in duodenal activity paralleled SO activity. Our results suggest that propofol in low doses may be useful for sedation during Sphincter of Oddi manometry in humans. Further studies of the effects of propofol on the human sphincter of Oddi are warranted.

Background Large-scale epidemiological studies support an important role for susceptibility genes in the pathogenesis of ischemic stroke, with phosphodiesterase 4D identified as the first gene predisposing to ischemic stroke. Several single nucleotide polymorphisms within the phosphodiesterase 4D gene have been implicated in the pathogenesis of stroke. Aim Undertake a multivariate analysis of six single nucleotide polymorphisms within the phosphodiesterase 4D gene in a previously defined Australian stroke cohort, to determine whether these single nucleotide polymorphisms have an association with ischemic stroke. Methods This case–control study was performed using an existing genetic database of 180 ischemic stroke patients and 301 community controls, evaluated previously for cerebrovascular risk factors (hypertension, hypercholesterolemia, diabetes, paroxysmal atrial fibrillation, smoking and history of stroke in a first-degree relative). Based on previously reported associations with large vessel disease, ischemic stroke, cardioembolic stroke or a mixture of these, six single nucleotide polymorphisms in the phosphodiesterase 4D gene were selected for study, these being single nucleotide polymorphisms 13, 19, rs152312, 45, 83 and 87, based on previously utilized DeCODE nomenclature. Single nucleotide polymorphisms were genotyped using a sequence-specific polymerase chain reaction method and gel electrophoresis. Logistic regression was undertaken to determine the relevance of each polymorphism to stroke. Further analysis was undertaken to determine the risk of stroke following stratification for stroke sub-type and etiology. Results Significant odds ratios were found to be associated with cardioembolic strokes in two single nucleotide polymorphisms: rs152312 and SNP 45 ( PConclusions Our findings demonstrated an association between cardioembolic stroke and phosphodiesterase 4D single nucleotide polymorphisms rs152312 and 45. No significant association was found for the other four single nucleotide polymorphisms investigated within the phosphodiesterase 4D gene. We propose that the results from this Australian population support the concept that a large prospective international study is required to investigate the role of phosphodiesterase 4D in the cardiogenic cause of ischemic stroke.

The objective of this study was to determine whether fine particulate organic matter (FPOM) from different sources would have similar surface areas. Individual FPOM particles collected from Grasshopper Creek (clear-cut), Mack Creek (old-growth coniferous forest), and Quartz Creek (second-growth) in Oregon were photographed using scanning electron microscopy, and their surface area was calculated by assuming spherical or cylindrical shapes. In Grasshopper Creek, FPOM cylinders (n = 326) represented 89% of the total surface area (124.9 m 2 ) and 68% of the total FPOM numbers. In Mack Creek, FPOM cylinders (n = 231) contributed 77% of the total surface area (114.2 m 2 ) even though they represented only 55% of the total numbers. In Quartz Creek, FPOM cylinders (n = 185) represented 79% of the total surface area (61.8 m 2 ) and 60% of the total numbers. There was a significant difference in the distribution of particle sizes and shapes from the different streams, particularly betwee...

Colonies of the bryozoan Pectinatella magnifica commonly occur on submersed substrata in an oxbow lake (Touson Lake) in the floodplain of the Black Warrior River, Alabama. Seasonal growth patterns, substratum preference, and potential effects of bryozoan colonies on algal assem- blages attached to artificial and natural substrata were determined. Colony growth on artificial substrata (pine sticks) and natural ones (dead cypress twigs and aquatic plants) was monitored at biweekly intervals from the appearance of bryozoans during early autumn to the loss of colonies from substrata in late December. Maximum colony growth occurred during late September and early October. Some colonies reached up to 65 cm in length and 10 cm in diameter. Colonies showed no preference among the substrata examined, but young colonies always developed first on the shaded side of the substratum. The presence of bryozoan colonies affected the composition of attached algae. Blue-green algae (90%) dominated on surfaces enclosed by the colonies and also within the gelatinous colony matrix, whereas surfaces uncolonized by Bryozoa developed mixed communities of diatoms (78%), blue-green algae (12%), and green algae (11%).

(1991). Community studies in an old-growth stream ecosystem in the Mobile River Basin, Alabama, USA. SIL Proceedings, 1922-2010: Vol. 24, No. 3, pp. 1664-1669.

This paper reports on the investigation conducted by Antwerp Water Works (AWW) in Belgium to make a long term (12 months) comparison between SBF and high-rate DAF to determine which process would be optimal. Three major objectives where put forward at the beginning of the study: technology comparison, gain operational experience and conduct coagulant testing. This paper discusses the result obtained with respect to these objectives. Overall this paper clearly points to the value this type of piloting can bring to water companies.

Summary 1. Species-discharge relationships (SDR) are aquatic analogues of species-area relationships, and are increasingly used in both basic research and conservation planning. SDR studies are often limited, however, by two shortcomings. First, they do not determine whether reported SDRs, which normally use complete drainage basins as sampling units, are scale dependent. Second, they do not account for the effects of habitat diversity within or among samples. 2. We addressed both problems by using discrete fish zones as sampling units in a SDR analysis. To do so, we first tested for longitudinal zonation in three rivers in the southeastern U.S.A. In each river, we detected successive ‘lower’, ‘middle’, and ‘upper’ fish zones, which were characterized by distinct fish assemblages with predictable habitat requirements. Because our analyses combined fish data from multiple sources, we also used rarefaction and Monte Carlo simulation to ensure that our zonation results were robust to spurious sampling effects. 3. Next, we estimated the average discharge within each zone, and plotted these estimates against the respective species richness within each zone (log10 data). This revealed a significant, linear SDR (r2 = 0.83; P

Vascular smooth muscle cell (VSMC) proliferation is an important etiological factor in vascular proliferative diseases such as primary atherosclerosis, hypertension, arterial and in-stent restenosis, and transplant vasculopathy. Our studies established that butyrate, a bacterial fermentation product of dietary fiber and a chromatin modulator, is a potent inhibitor of VSMC proliferation. The cardiovascular health benefits of a high-fiber diet, the principle source of butyrate in the body, have been known for a long time, however, very little is known about the antiatherogenic potential of butyrate. Because oxidative stress plays an important role in the pathogenesis of atherosclerosis, we examined involvement of the glutathione/glutathione S-transferase (GST) antioxidant system in butyrate's inhibition of VSMC proliferation. Treatment of proliferating VSMCs with butyrate leads to the induction of several GSTs. Interestingly, our study also demonstrated the nuclear localization of GST-P1 (GST-7-7), which is considered to be a cytosolic protein; this was demonstrated using immunostaining and was corroborated by western blotting. Also, the butyrate-induced antiproliferative action, and the induction of GST-P1 and its nuclear localization are downregulated when butyrate is withdrawn. Furthermore, assessment of intracellular glutathione levels reveals their augmentation by butyrate. Conversely, butyrate treatment reduces the levels of reactive oxygen species in VSMCs. Collectively, the butyrate-treatment-related increase in glutathione content, the reduction in reactive oxygen species, the upregulation of GST and the nuclear localization of GST-P1 in growth-arrested VSMCs imply that butyrate's antiproliferative action involves modulation of the cellular redox state. Thus, induction of the glutathione/GST antioxidant system appears to have other regulatory role(s) besides detoxification and regulation of the cellular redox state, for example, cell-cycle control and cell proliferation, which are both critical to atherogenesis.

Vascular access polytetrafluoroethylene (PTFE) graft failure is a major cause of morbidity in the hemodialysis population. The most common cause of graft failure is thrombosis secondary to stenosis at the venous outflow tract. Venous outflow stenosis is characterized by intimal-medial hyperplasia. We have developed a porcine arteriovenous (AV) graft model that may be used to investigate this proliferative response and aid in the development of new therapies to prevent intimal-medial hyperplasia and improve graft patency.Left carotid to right external jugular vein PTFE (6 mm) grafts were implanted in the necks of swine. Immediately following anatomosis, flow rates were recorded. In one group of animals (n = 4) the venous outflow tract was harvested after 7 days and morphometric analysis of intimal and medial area was performed. In a second group (n = 8) the graft patency was monitored until 28 days.All porcine PTFE fistula grafts were patent at 7 days and 100% patency was maintained until 14 days. After 28 days, 75% of the grafts failed due to thrombosis. The venous outflow tract developed a significant proliferative response. After 7 days the intimal and medial areas were 469 +/- 9 microm2 and 875 +/- 26 microm2 respectively. At 28 days the intimal and medial areas were 913 +/- 55 microm2 and 1437 +/- 182 microm2 respectively. Luminal flow rate of the venous outflow tract was reduced significantly (344 +/- 11 ml/min at Day 0 to 129 +/- 14 ml/min at Day 7, p0.05).This porcine model rapidly, reliably and robustly reproduces the flow reducing stenosis and intimal-medial hyperplasia at the venous outflow tract of PTFE arteriovenous fistula. It represents a promising tool for investigating the mechanisms of intimal-medial hyperplasia, evaluating therapeutic interventions and new graft materials.

This article provides the complete description of resultsfrom the Phase I data set of the Sudbury Neutrino Observatory (SNO). ThePhase I data set is based on a 0.65 kt-year exposure of heavy water tothe solar 8B neutrino flux. Included here are details of the SNO physicsand detector model, evaluations of systematic uncertainties, andestimates of backgrounds. Also discussed are SNO's approach tostatistical extraction of the signals from the three neutrino reactions(charged current, neutral current, and elastic scattering) and theresults of a search for a day-night asymmetry in the ?e flux. Under theassumption that the 8B spectrum is undistorted, the measurements fromthis phase yield a solar ?e flux of ?(?e) =1.76+0.05?0.05(stat.)+0.09?0.09 (syst.) x 106 cm?2 s?1, and a non-?ecomponent ?(? mu) = 3.41+0.45?0.45(stat.)+0.48?0.45 (syst.) x 106 cm?2s?1. The sum of these components provides a total flux in excellentagreement with the predictions of Standard Solar Models. The day-nightasymmetry in the ?e flux is found to be Ae = 7.0 +- 4.9 (stat.)+1.3?1.2percent (sys.), when the asymmetry in the total flux is constrained to bezero.

ObjectiveVascular access dysfunction is a major problem in hemodialysis patients. Only 50% of arteriovenous grafts (AVGs) will remain patent 1 year after surgery. AVGs frequently develop stenoses and occlusions at the venous anastomoses in the venous outflow tract. Lumen diameter is not only determined by intimal thickening but is also influenced by remodeling of the vessel wall. Vascular remodeling requires degradation and reorganization of the extracellular matrix by the degradation enzymes, matrix metalloproteinases (MMPs). In this study, we aimed to provide further insight into the mechanism of endothelial regulation of vascular remodeling and luminal narrowing in AVGs.MethodsEnd-to-side carotid artery–jugular vein polytetrafluoroethylene grafts were created in 20 domestic swine. The anastomoses and outflow vein were treated with Gelfoam matrices (Pfizer, New York, NY) containing allogeneic porcine aortic endothelial (PAE, n = 10) cells or control matrices without cells (n = 10), and the biologic responses to PAE implants were investigated 3 and 28 days postoperatively. Angiograms before euthanasia were compared with baseline angiograms. Tissue sections were stained with hematoxylin and eosin, Verhoeff elastin, and antibodies specific to MMP-9 and MMP-2 and underwent histopathologic, morphometric and immunohistochemical analysis.ResultsVeins treated with PAE cell implants had a 2.8-fold increase in venous lumen diameter compared with baseline (P < .05), a 2.3-fold increase in lumen diameter compared with control, and an 81% decrease in stenosis (P < .05) compared with control at 28 days. The increase in lumen diameter by angiographic analysis correlated with morphometric analysis of tissue sections. PAE implants increased the venous lumen area 2.3-fold (P < .05), decreased venous luminal occlusion 66%, and increased positive venous remodeling 1.9-fold (P < .05) compared with control at 28 days. PAE cell implants reduced MMP-2 expression and neovascularization at 3 and 28 days and adventitial fibrosis at 28 days, suggesting a role of the implants in controlling the affects of medial and adventitial cells in the response to vascular injury.ConclusionsThese results demonstrate that the adventitial application of endothelial implants significantly reduced MMP-2 expression within the venous wall, and increased venous lumen diameter and positive remodeling in a porcine arteriovenous graft model. Adventitial endothelial implants may be useful in decreasing luminal narrowing in a clinical setting.Clinical RelevanceVascular access dysfunction is the leading cause of hospitalization and morbidity in patients receiving hemodialysis for end-stage renal disease. Data indicate that most arteriovenous grafts fail due to the formation of stenosis at the vein-graft anastomotic and venous outflow sites. The stenoses result in luminal narrowing and subsequent graft thrombosis and failure. A satisfactory long-term pharmacologic means of preventing stenosis due to intimal hyperplasia and negative remodeling in hemodialysis grafts has yet to be found. In a large animal model of arteriovenous grafts, we show that placement of an adventitial endothelial implant significantly increased venous lumen diameter at 28 days.

Acrolein, an environmental pollutant and a lipid peroxidation product, is implicated in vascular pathogenesis. Although evidence indicates a link between vascular pathogenesis and acrolein, no direct studies relating to effects of acrolein on vascular function and responses are known. This study investigated the effects of acrolein on vascular function to understand the underlying mechanism of acrolein-induced vascular responses. Male Sprague-Dawley rats were treated with acrolein (2 or 4 mg/kg; i.p.) for 3 or 7 days. Urine and blood samples were collected. Changes in systolic blood pressure (SBP) and responses to acetylcholine and phenylephrine were determined. Acrolein (4 mg/kg, 7 days) significantly increased SBP by 25%, phenylephrine vasoconstriction by 2-fold, but decreased urinary excretion of nitrite by 25%. Acrolein inhibited generation of cyclic guanosine 3'5'-monophosphate (cGMP) by 98%, and did not alter expression of nitric oxide synthase (eNOS). Acrolein increased the generation of lipid hydroperoxide in plasma and aortic tissue by 21% and 124% respectively, increased glutathione-S-transferase (GST) and glutathione peroxidase (GSH-Px) activities. Acrolein up-regulated the expression of GST by 2 fold. These data suggest that induced SBP and altered vasoconstriction/vasodilatation in acrolein treated rats may be due to reduced availability of NO via increased free radical generation and reduced antioxidant defense.

Total mercury (THg) and mono-methylmercury (MeHg) levels in water, sediment, and largemouth bass (LMB) (Micropterus salmoides) were investigated at 52 sites draining contrasting land use/land cover and habitat types within the Mobile Alabama River Basin (MARB). Aqueous THg was positively associated with iron-rich suspended particles and highest in catchments impacted by agriculture. Sediment THg was positively associated with sediment organic mater and iron content, with the highest levels observed in smaller catchments influenced by wetlands, followed by those impacted by agriculture or mixed forest, agriculture, and wetlands. The lowest sediment THg levels were observed in main river channels, except for reaches impacted by coal mining. Sediment MeHg levels were a positive function of sediment THg and organic matter and aqueous nutrient levels. The highest levels occurred in agricultural catchments and those impacted by elevated sulfate levels associated with coal mining. Aqueous MeHg concentrations in main river channels were as high as those in smaller catchments impacted by agriculture or wetlands, suggesting these areas were sources to rivers. Elevated Hg levels in some LMB were observed across all types of land use and land cover, but factors such as shallow water depth, larger wetland catchment surface area, low aqueous potassium levels, and higher Chl a concentrations were associated with higher Hg burdens, particularly in the Coastal Plain province. It is suggested that the observed large variability in LMB Hg burdens is linked to fish displacement by anglers, differences in food web structure, and sediment biogeochemistry, with surficial sediment iron oxides buffering the flux of MeHg from sediments to deeper water pelagic food webs.

Excessive proliferation of vascular smooth muscle cells (VSMCs) is a critical element in the development of several vascular pathologies, particularly in atherosclerosis and in restenosis due to angioplasty. We have shown that butyrate, a powerful antiproliferative agent, a strong promoter of cell differentiation and an inducer of apoptosis inhibits VSMC proliferation at physiological concentrations with no cytotoxicity. In the present study, we have used cDNA array technology to unravel the molecular basis of the antiproliferative effect of butyrate on VSMCs. To assess the involvement of gene expression in butyrate-inhibited VSMC proliferation, proliferating VSMCs were exposed to 5 mmol/l butyrate 1 through 5 days after plating. Expression profiles of 1.176 genes representing different functional classes in untreated control and butyrate treated VSMCs were compared. A total of 111 genes exhibiting moderate (2.0-5.0 fold) to strong (5.0 fold) differential expression were identified. Analysis of these genes indicates that butyrate treatment mainly alters the expression of four different functional classes of genes, which include: 43 genes implicated in cell growth and differentiation, 13 genes related to stress response, 11 genes associated with vascular function and 8 genes normally present in neuronal cells. Examination of differentially expressed cell growth and differentiation related genes indicate that butyrate-inhibited VSMC proliferation appears to involve down-regulation of genes that encode several positive regulators of cell growth and up-regulation of some negative regulators of growth or differentiation inducers. Some of the down-regulated genes include proliferating cell nuclear antigen (PCNA), retinoblastoma susceptibility related protein p130 (pRb), cell division control protein 2 homolog (cdc2), cyclin B1, cell division control protein 20 homolog (p55cdc), high mobility group (HMG) 1 and 2 and several others. Whereas the up-regulated genes include cyclin D1, p21WAF1, p141NK4B/p15INK5B, Clusterin, inhibitor of DNA binding 1 (ID1) and others. On the other hand, butyrate-responsive stress-related genes include some of the members of heat shock protein (HSP), glutathione-s-transferase (GST), glutathione peroxidase (GSH-PXs) and cytochrome P450 (CYP) families. Additionally, several genes related to vascular and neuronal function are also responsive to butyrate treatment. Although involvement of genes that encode stress response, vascular and neuronal functional proteins in cell proliferation is not clear, cDNA expression array data appear to suggest that they may play a role in the regulation of cell proliferation. However, cDNA expression profiles indicate that butyrate-inhibited VSMC proliferation involves combined action of a proportionally large number of both positive and negative regulators of growth, which ultimately causes growth arrest of VSMCs. Furthermore, these butyrate-induced differential gene expression changes are not only consistent with the antiproliferative effect of butyrate but are also in agreement with the roles that these gene products play in cell proliferation.

Acrolein, a major component of cigarette smoke, an environmental pollutant and an endogenous lipid peroxidation product, has been implicated in the development of atherosclerosis. Although a link between vascular injury and acrolein has been indicated, the exact molecular mechanism of acrolein-induced toxicity to vasculature is unknown. In an effort to elucidate the molecular basis of acrolein-induced vascular toxicity, the possibility of the intracellular signaling system as one of the targets of acrolein-induced toxicity is investigated in the present study. Exposure of cultured rat vascular smooth muscle cells (VSMCs) to different doses of acrolein not only causes cytotoxicity but also alters cellular morphology in a concentration and time-dependent manner. VSMCs exhibit cytotoxicity to a narrow concentration range of 5-10 microg/ml and display no toxicity to 2 microg/ml acrolein even after 24 h of exposure. Furthermore, exposure to acrolein results in activation of members of the mitogen-activated protein kinase (MAPK) family and protein tyrosine kinases. The extracellular signal-regulated kinases 1 and 2 (ERK1/2), stress-activated protein kinases/c-jun NH2-terminal kinases (SAPK/JNK) and p38MAPK are effectively and transiently activated by acrolein in a concentration and time-dependent fashion. While all three MAPKs exhibit significant activation within 5 min of exposure to acrolein, maximum activation (ERK1/2 and p38MAPK) or close to maximum activation (SAPK/JNK) occurs on exposure to 5 microg/ml acrolein for 2 h. Acrolein-induced activation of MAPKs is further substantiated by the activation of transcription factors, c-jun and activator transcription factor-2 (ATF-2), by acrolein-activated SAPK/JNK and p38MAPK, respectively. Additionally several cellular proteins exhibit spectacular protein tyrosine phosphorylation, particularly in response to 2 and 5 microg/ml of acrolein. Interestingly, the acrolein-induced activation of MAPKs precedes acrolein-stimulated protein tyrosine phosphorylation, which occurs after 2 h of exposure to acrolein. However, the time course of maximum protein tyrosine phosphorylation profile corresponds to the peak activation profile of MAPKs. The activation of MAPKs and protein tyrosine phosphorylation by acrolein appears to be independent of acrolein-induced toxicity. VSMCs exposed to 2 microg/ml acrolein exhibit no toxicity but stimulates significant activation of MAPKs and protein tyrosine phosphorylation. Although acrolein-induced VSMC toxicity is not blocked by MAPK inhibitors, PD98059, an inhibitor of MAPK kinase and SB203580, an inhibitor of p38MAPK, eitheralone or in combination, each MAPK responds differently to the inhibitors. Most prominently, although SB203580, an inhibitor of both SAPK/JNK and p38MAPK, significantly inhibited acrolein-induced activation of p38MAPK, it also stimulated SAPK/JNK activation by acrolein alone and in combination with PD98059. These results provide the first evidence that the activation of both growth-regulated (ERK1/2) and stress-regulated (SAPK/JNK and p38MAPK) MAPKs as well as tyrosine kinases are involved in the mediation of acrolein-induced effects on VSMC, which may play a crucial role in vascular pathogenesis due to environmentally and endogenously produced acrolein.