Sensitivity Of Quagga Mussels (dreissena Rostriformis Bugensis) To Cyanobacteria At Multiple Life History Stages

Quagga mussels (Dreissena rostriformis bugensis) originate from brackish waters of the Ponto-Caspian area and are nuisance invasive species in North American and European freshwaters. Their invasion has caused major economic and ecological damages in the Laurentian Great Lakes. Through selective filter feeding, quagga mussels have promoted the growth of cyanobacteria. Harmful cyanobacteria blooms have the potential to produce toxins, which can be toxic to humans and wildlife. Although quagga mussels can increase the prevalence of cyanobacteria blooms, it is unknown how they are physiologically affected by cyanobacteria and understanding these dynamics can be useful in the management of this invasive species. To evaluate the effects of cyanobacteria on quagga mussels, I evaluated reproduction, early development, and physiological and cellular stress in several laboratory studies. Sperm motility was assessed using a novel optical bioassay to record sperm movement and measure distance, velocity, and acceleration of individual sperm cells in the presence of eleven cyanobacteria cultures and the purified cyanotoxin, microcystin. Sperm motility was reduced in the presence of four cyanobacteria cultures, but was unaffected by microcystin. Next, I evaluated spawning success by inducing quagga mussels to spawn using serotonin and exposing them to thirteen cyanobacteria cultures and found one culture of Aphanizomenon flos-aquae hinders gamete release. I then combined quagga mussel sperm and eggs in cyanobacteria solution to determine if cyanobacteria would prevent successful fertilization and found six cultures reduced fertilization rates compared to the control. To determine how cyanobacteria influence the sensitive larval veliger stage of dreissenid mussels, I collected veligers off shore from the Detroit River, MI, USA and observed mortality in the presence of five concentrations of eleven cyanobacteria cultures and microcystin. In a series of bioassays, I then determined a dose response curve for each cyanobacteria culture and microcystin and found that veligers experience high mortality rates when exposed to environmentally relevant concentrations of cyanobacteria and cyanotoxins. Results from these experiments can be used to create management techniques that target invasive quagga mussels at their most sensitive life history stages. Finally, I explored how the brackish origins of quagga mussels impact their metabolism and oxidative stress response in freshwater systems by comparing them to another freshwater invasive bivalve, the Asian clam (Corbicula fluminea) when exposed to cyanobacteria and microcystin stressors. My results support previous work that brackish to freshwater invasion can act as a context dependent form of stress and result in higher respiration and filtration rates and altered oxidative stress response. The findings from these studies can be used to predict invasive species distribution and range expansion and can lead to more effective control of nuisance populations

Particulate Matter Exposure Impairs Systemic Microvascular Endothelium-Dependent Dilation

Acute exposure to airborne pollutants, such as solid particulate matter (PM), increases the risk of cardiovascular dysfunction, but the mechanisms by which PM evokes systemic effects remain to be identified. The purpose of this study was to determine if pulmonary exposure to a PM surrogate, such as residual oil fly ash (ROFA), affects endothelium-dependent dilation in the systemic microcirculation. Rats were intratracheally instilled with ROFA at 0.1, 0.25, 1 or 2 mg/rat 24 hr before experimental measurements. Rats intratracheally instilled with saline or titanium dioxide (0.25 mg/rat) served as vehicle or particle control groups, respectively. In vivo microscopy of the spinotrapezius muscle was used to study systemic arteriolar dilator responses to the Ca(2+) ionophore A23187, administered by ejection via pressurized micropipette into the arteriolar lumen. We used analysis of bronchoalveolar lavage (BAL) samples to monitor identified pulmonary inflammation and damage. To determine if ROFA exposure affected arteriolar nitric oxide sensitivity, sodium nitroprusside was iontophoretically applied to arterioles of rats exposed to ROFA. In saline-treated rats, A23187 dilated arterioles up to 72 ± 7% of maximum. In ROFA- and TiO(2)-exposed rats, A23187-induced dilation was significantly attenuated. BAL fluid analysis revealed measurable pulmonary inflammation and damage after exposure to 1 and 2 mg ROFA (but not TiO(2) or < 1 mg ROFA), as evidenced by significantly higher polymorphonuclear leukocyte cell counts, enhanced BAL albumin levels, and increased lactate dehydrogenase activity in BAL fluid. The sensitivity of arteriolar smooth muscle to NO was similar in saline-treated and ROFA-exposed rats, suggesting that pulmonary exposure to ROFA affected endothelial rather than smooth muscle function. A significant increase in venular leukocyte adhesion and rolling was observed in ROFA-exposed rats, suggesting local inflammation at the systemic microvascular level. These results indicate that pulmonary PM exposure impairs systemic endothelium-dependent arteriolar dilation. Moreover, because rats exposed to < 1 mg ROFA or TiO(2) did not exhibit BAL signs of pulmonary damage or inflammation, it appears that PM exposure can impair systemic microvascular function independently of detectable pulmonary inflammation

Systemic Microvascular Dysfunction and Inflammation after Pulmonary Particulate Matter Exposure

The epidemiologic association between pulmonary exposure to ambient particulate matter (PM) and cardiovascular dysfunction is well known, but the systemic mechanisms that drive this effect remain unclear. We have previously shown that acute pulmonary exposure to PM impairs or abolishes endothelium-dependent arteriolar dilation in the rat spinotrapezius muscle. The purpose of this study was to further characterize the effect of pulmonary PM exposure on systemic microvascular function and to identify local inflammatory events that may contribute to these effects. Rats were intratracheally instilled with residual oil fly ash (ROFA) or titanium dioxide at 0.1 or 0.25 mg/rat 24 hr before measurement of pulmonary and systemic microvascular responses. In vivo microscopy of the spinotrapezius muscle was used to study systemic arteriolar responses to intraluminal infusion of the Ca(2+) ionophore A23187 or iontophoretic abluminal application of the adrenergic agonist phenylephrine (PHE). Leukocyte rolling and adhesion were quantified in venules paired with the studied arterioles. Histologic techniques were used to assess pulmonary inflammation, characterize the adherence of leukocytes to systemic venules, verify the presence of myeloperoxidase (MPO) in the systemic microvascular wall, and quantify systemic microvascular oxidative stress. In the lungs of rats exposed to ROFA or TiO(2), changes in some bronchoalveolar lavage markers of inflammation were noted, but an indication of cellular damage was not found. In rats exposed to 0.1 mg ROFA, focal alveolitis was evident, particularly at sites of particle deposition. Exposure to either ROFA or TiO(2) caused a dose-dependent impairment of endothelium-dependent arteriolar dilation. However, exposure to these particles did not affect microvascular constriction in response to PHE. ROFA and TiO(2) exposure significantly increased leukocyte rolling and adhesion in paired venules, and these cells were positively identified as polymorphonuclear leukocytes (PMNLs). In ROFA- and TiO(2)-exposed rats, MPO was found in PMNLs adhering to the systemic microvascular wall. Evidence suggests that some of this MPO had been deposited in the microvascular wall. There was also evidence for oxidative stress in the microvascular wall. These results indicate that after PM exposure, the impairment of endothelium-dependent dilation in the systemic microcirculation coincides with PMNL adhesion, MPO deposition, and local oxidative stress. Collectively, these microvascular observations are consistent with events that contribute to the disruption of the control of peripheral resistance and/or cardiac dysfunction associated with PM exposure

Social Class

Discussion of class structure in fifth-century Athens, historical constitution of theater audiences, and the changes in the comic representation of class antagonism from Aristophanes to Menander

THE ROLE OF OXYGEN IN ESCAPE OF SKELETAL MUSCLE ARTERIOLES FROM SYMPATHETIC NERVE STIMULATION (MICROCIRCULATION, BLOOD FLOW).

In these experiments, we tested the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell oxygen levels following blood flow reduction. This hypothesis predicts that if the fall in parenchymal cell PO₂ during stimulation can be minimized, escape should be reduced. To test this prediction, we studied the behavior of superficial arterioles of the cat sartorius muscle during 3 minutes of sympathetic nerve stimulation. The muscle was covered with silicone oil equilibrated with 0%, 5% and 10% oxygen. During stimulation under 0% oxygen, 90% of visible arterioles showed a significant secondary relaxation (escape). The relaxation averaged 55% of the initial constriction. Under 5% oxygen, resting arteriolar diameter was reduced by an average of 12% and escape was significantly reduced throughout the arteriolar network. Under 10% ambient oxygen, there was an additional 5% reduction in resting diameter and a further reduction of escape. Escape was not attenuated when control diameter was reduced to the same degree with arginine vasopressin, suggesting that the effect of oxygen was specific rather than secondary to an increase in vascular tone. The above observations are also consistent with the hypothesis that escape is mediated through a fall in vascular wall PO₂. To evaluate this possibility, periarteriolar and parenchymal tissue PO₂ were measured with oxygen microelectrodes during sympathetic stimulation under 0% and 10% oxygen suffusion of the muscle. In the proximal arterioles, the periarteriolar PO₂ during control and during stimulation was identical under 0% and 10% oxygen yet escape was reduced by 75% under 10% oxygen. Similarly, escape was reduced 90% in the distal arterioles under 10% oxygen but periarteriolar PO₂ was very nearly the same as that measured under 0% oxygen. In contrast, mean parenchymal tissue PO₂ fell to low levels during stimulation under 0% oxygen but did not fall below normal levels during stimulation under 10% oxygen. These findings argue against the hypothesis that a fall in vascular wall PO₂ is responsible for escape. The findings are consistent with the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell PO₂. (Abstract shortened with permission of author.

Beiträge zur Pathologie der Lues

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