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PubMed1998

Prevention of cellular edema directly caused by hypothermic cardioplegia: studies in isolated human and rabbit atrial myocytes.

OBJECTIVES: This study tested the hypothesis that edema during hypothermic cardioplegia is caused by the hypotonicity of the perfusate at cold temperatures. METHODS: The volume of isolated human and rabbit atrial myocytes was measured by video microscopy under nonischemic conditions. Each cell served as its own control. RESULTS: After equilibration in 37 degrees C physiologic buffer (Tyrode's solution), exposure to 9 degrees C St. Thomas' Hospital solution for 20 minutes caused human atrial cells to swell by 20% and rabbit atrial cells to swell by 10%. Cell volume fully recovered on rewarming in 37 degrees C physiologic solution. Cell swelling was due to the composition of St. Thomas' Hospital solution rather than hypothermia alone. Exposure to 9 degrees C physiologic solution did not significantly affect cell volume. Swelling of myocytes was largely prevented by replacing most of the Cl- in St. Thomas' Hospital solution with an impermeant anion so that the product of the concentrations of K+ and Cl- were the same as in the physiologic solution. CONCLUSIONS: This study suggests that cell swelling during hypothermic cardioplegia is caused in part by the composition of the cardioplegic solution. The volume of cardiac myocytes appears to follow a Donnan equilibrium in the cold, and the perfusate KCl product determines water movement. Thus, the tonicity of hyperkalemic cardioplegic solutions can be adjusted to a physiologic value by replacing most Cl- by an impermeant anion. Following this simple principle, a reformulation of cardioplegic solutions may be able to minimize iatrogenic myocardial edema.

Adult↗

PubMed2002

Enhanced endogenous thrombolysis induced by a specific factor Xa inhibitor, DX-9065a, evaluated in a rat arterial thrombolysis model in vivo.

We have previously established an animal model to investigate mechanisms of arterial thrombolysis in vivo and have demonstrated that endogenous thrombolysis, mediated by thrombin-activatable fibrinolysis inhibitor, is enhanced by administration of specific thrombin inhibitors. The aim of the present study was to evaluate the effects of a synthetic and specific factor Xa inhibitor, DX-9065a, on endogenous fibrinolysis. Mural thrombi were formed in rat mesenteric arterioles by helium-neon laser irradiation in the presence of Evans blue. Thrombolysis was continuously monitored by video microscopy and was quantified using image analysis software. Oral and intravenous administration of DX-9065a enhanced endogenous thrombolysis in vivo. The mechanisms require additional investigation using other experimental systems, but nevertheless, the present results extended our previous findings and further suggested that the enhanced fibrinolysis might be due to depressed activity thrombin-activatable fibrinolysis inhibitor. The synthetic factor Xa inhibitor could provide the basis for a useful thrombolytic agent.

Administration, Oral↗

PubMed1997

Increases in cytosolic Ca2+ accompany basophil activation by eosinophil granule major basic protein.

The response of basophil cytosolic free Ca2+ concentrations ([Ca2+]i) to stimulation by eosinophil granule major basic protein (MBP) was assessed using digital video microscopy. MBP stimulated an elevation in basophil [Ca2+]i that, in general, developed slowly and increased monotonically. In some experiments, however, the average rise in [Ca2+]i was biphasic, with an initial transient increase followed by a larger and more sustained elevation. At the single cell level MBP stimulation caused frequent, asynchronous oscillations in [Ca2+]i that ranged up to 300 nM in amplitude. Chelation of extracellular Ca2+ selectively blocked the second, sustained rise in [Ca2+]i as well as MBP-induced histamine release. Within individual experiments, the increase in [Ca2+]i paralleled the level of histamine release. These results demonstrate that, unlike the activation of neutrophils or eosinophils, basophil activation by MBP correlates with an elevation in [Ca2+]i. Further, the MBP induced [Ca2+]i response exhibits several features in common with the IgE-mediated [Ca2+]i response.

Basophils↗

PubMed2001

Drug targeting using thermally responsive polymers and local hyperthermia.

We report a new thermal targeting method in which a thermally responsive drug carrier selectively accumulates in a solid tumor that is maintained above physiological temperature by externally applied, focused hyperthermia. We synthesized two thermally responsive polymers that were designed to exhibit a lower critical solution temperature (LCST) transition slightly above physiological temperature: (1) a genetically engineered elastin-like polypeptide (ELP) and (2) a copolymer of N-isopropylacrylamide (NIPAAm) and acrylamide (AAm). The delivery of systemically injected polymer-rhodamine conjugates to solid tumors was investigated by in vivo fluorescence video microscopy of ovarian tumors implanted in dorsal skin fold window chambers in nude mice, with and without local hyperthermia. When tumors were heated to 42 degrees C, the accumulation of a thermally responsive ELP with a LCST of 40 degrees C was approximately twofold greater than the concentration of the same polymer in tumors that were not heated. Similar results were also obtained for a thermally responsive poly(NIPAAM-co-AAm), though the enhanced accumulation of this carrier in heated tumors was lower than that observed for the thermally responsive ELP. These results suggest that enhanced delivery of drugs to solid tumors can be achieved by conjugation to thermally responsive polymers combined with local heating of tumors.

Acrylamides↗

PubMed1999

Characterization of ion transport mechanisms involved in bombesin-stimulated biliary secretion in rat cholangiocytes.

BACKGROUND/AIMS: Bombesin is a neuropeptide which stimulates fluid and bicarbonate secretion from cholangiocytes by stimulating Cl-/HCO3- exchange. However, the underlying regulation and interactions of ion transporters and channels mediating this bombesin-stimulated biliary secretion are not well characterized. The aim of the study was to characterize the ion transport processes involved in bombesin-stimulated secretion in polarized cholangiocytes in comparison with those of secretin. METHODS: Isolated bile duct units (IBDU) were prepared from normal rat liver. Biliary secretion induced by bombesin was measured by quantitative video-microscopy in the presence and absence of inhibitors. RESULTS: Bombesin-stimulated secretion was inhibited by H2-DIDS, NPPB, BaCl2, TEA, and acetazolamide. However, in contrast to secretin, bombesin-stimulated secretion was not inhibited by disruption of microtubules. CONCLUSIONS: Bombesin-stimulated biliary secretion is dependent on anion exchangers, Cl- and K+ channels, and carbonic anhydrase but not on microtubules. Bombesin regulates secretion in cholangiocytes by different mechanisms from those established for secretin.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed2003

Contrast agent bubble and erythrocyte behavior in a 1.5-MHz standing ultrasound wave.

Human erythrocytes and Optison contrast agent have been exposed to ultrasound, both alone and in combination, in a single-half-wavelength chamber driven at its resonance frequency (fo) of 1.5 MHz. Cell movements were recorded by video microscopy at speeds up to 500 frames/s. The hypothesis that cells near a standing wave pressure node might be stressed by the microbubble products of sonicated contrast agent was examined. In the absence of contrast agent, cells moved rapidly to form an aggregate in the standing wave pressure node plane. First subharmonic and second harmonic emissions were detected from cell-contrast agent suspensions immediately on exposure to a threshold peak pressure amplitude of 0.98 MPa. Emissions at 3fo/2 occurred at 1.47 MPa, whereas white noise and lower-order subharmonic emissions coincided with the appearance of visible bubbles at a threshold of approximately 1.96 MPa. Cells exposed together with contrast agent at a pressure of 0.98 MPa precessed very rapidly about the pressure node plane. This behavior was discussed in the context of a recent analysis predicting that, in contrast to the situation for lower-pressure amplitudes, subresonant size bubbles translate about pressure node plane if the driving pressure amplitude is sufficiently high. Many precessing erythrocytes were clearly spiculated and this morphology persisted after the cells had left the area of precession. Hemoglobin release was significant under conditions inducing precession with first subharmonic and first harmonic emissions. Protein release increased discontinuously near the pressure thresholds, where more complex categories of frequency emission were detected. The potential of this system, which induces erythrocyte morphology changes and some protein release at the first emission threshold, to provide some control on the membrane-permeabilizing stress experienced by cells in a cavitation field is discussed.

Albumins↗

PubMed2002

Reversal of neuronal polarity characterized by conversion of dendrites into axons in neonatal rat cortical neurons in vitro.

The mechanisms for the establishment and maintenance of cell polarity in neurons are not well understood. Axon regeneration from dendrites has been reported after axotomy near the cell body in vivo. We report here in vitro a reversal of neuronal polarity characterized by the conversion of dendrites into axons. We isolated neurons from the neonatal rat cerebral cortex. Neurons that exhibited an apical dendrite with a length of >100 microm were monitored for 3 days in culture. In 66% of neurons examined, a new axon, as identified by reactivity with an antibody to dephosphorylated tau or by lack of reactivity with an antibody to the a and b isoforms of microtubule-associated protein 2, appeared to form from the tip of the original dendrite. Further analysis of such neurons revealed that the distal half of the original dendrite became positive for dephosphorylated tau or negative for microtubule-associated protein 2. Time-lapse video microscopy demonstrated the conversion of the original dendrite into an axon without dendritic retraction. Axon regeneration from dendritic tips required a significantly longer time than axon regeneration from minor processes. Our observations thus demonstrate in vitro a time-consuming reversal of neuronal polarity and the conversion of a dendritic cytoskeleton into an axonal one.

Actins↗

PubMed1998

Ca2+-dependence and nifedipine-sensitivity of vascular tone and contractility in the isolated superfused spiral modiolar artery in vitro.

The regulation of the vascular diameter of the spiral modiolar artery may play a major role in the regulation of cochlear blood flow and tissue oxygenation since the spiral modiolar artery provides the main blood supply to the cochlea. The goal of the present study was to determine whether vascular tone and contractility of the spiral modiolar artery depend on the presence of extracellular Ca2+ and involves nifedipine-sensitive Ca2+ channels. The spiral modiolar artery was isolated and superfused in vitro and the diameter was measured continuously by video microscopy. Isolated segments of the spiral modiolar artery had an outer diameter of 61 +/- 3 microm (n = 59) and displayed vasomotion characterized by 5-15 clearly distinguishable constrictions per min. Removal of Ca2+ from the superfusion medium caused a reversible relaxation and cessation of vasomotion and was used to determine the magnitude of basal vascular tone. The basal vascular tone consisted of a sustained reduction of the vascular diameter to 95.1 +/- 0.3% (n = 51) of the maximal diameter in Ca2+-free medium. Nifedipine reduced the basal vascular tone with an IC50 of (1.1 +/- 0.3) x 10(-9)) M although 22% of the basal vascular tone was insensitive to nifedipine. Elevation of the K+ concentration from 3.6 to 150 mM caused a transient vasoconstriction which was dependent on the presence of extracellular Ca2+. Nifedipine fully inhibited K+-induced vasoconstriction with an IC50 of (2.0 +/- 0.7) x 10(-9) M. Norepinephrine (10(-4) M) caused a transient vasoconstriction and an increase of vasomotion at branch points of the spiral modiolar artery. Norepinephrine-induced vasoconstriction was fully inhibited in the absence of Ca2+ and partially inhibited by 10(-7) M nifedipine. These observations suggest that the spiral modiolar artery contains voltage-dependent nifedipine-sensitive Ca2+ channels which are involved in the maintenance of basal vascular tone as well as in the mediation of K+- and norepinephrine-induced contractility. Further, the data suggest that cytosolic Ca2+ stores, if present in the spiral modiolar artery, are of limited capacity compared to other vessels.

Animals↗

PubMed2000

Timing of CNS cell generation: a programmed sequence of neuron and glial cell production from isolated murine cortical stem cells.

Multipotent stem cells that generate both neurons and glia are widespread components of the early neuroepithelium. During CNS development, neurogenesis largely precedes gliogenesis: how is this timing achieved? Using clonal cell culture combined with long-term time-lapse video microscopy, we show that isolated stem cells from the embryonic mouse cerebral cortex exhibit a distinct order of cell-type production: neuroblasts first and glioblasts later. This is accompanied by changes in their capacity to make neurons versus glia and in their response to the mitogen EGF. Hence, multipotent stem cells alter their properties over time and undergo distinct phases of development that play a key role in scheduling production of diverse CNS cells.

Animals↗

PubMed1997

Neuronal polarity: vectorial cytoplasmic flow precedes axon formation.

Axon formation in multipolar neurons is believed to depend on the existence of precise sorting mechanisms for axonal membrane and membrane-associated proteins. Conclusive evidence in living neurons, however, is lacking. In the present study, we use light and video microscopy to address this issue directly. We show that axon formation is preceded by the appearance in one of the multiple neurites of (1) a larger growth cone, (2) a higher amount and greater transport of membrane organelles, (3) polarized delivery of TGN-derived vesicles, (4) a higher concentration of mitochondria and peroxisomes, (5) a higher concentration of a cytosolic protein, and (6) a higher concentration of ribosomes. These results provide evidence for the involvement of bulk cytoplasmic flow as an early determinant of neuronal morphological polarization. Molecular sorting events would later trigger the establishment of functional polarity.

Animals↗

PubMed2001

Dynamic intrahepatic flow and cellular alterations during radiofrequency ablation of liver tissue in mice.

PURPOSE: The purpose of this study was to identify microvascular and other associated changes that occur in the liver during focal heating with monopolar radiofrequency (RF). MATERIALS AND METHODS: Intravital video microscopy was performed on exteriorized transilluminated livers of 15 live mice during RF-induced heating of liver parenchyma. Microvascular flow parameters, flow reversibility, microbubble formation, phagocytic activity, and endothelial permeability were recorded throughout a range of tip temperatures (40 degrees C-95 degrees C). RESULTS: During RF application, five discrete zones extended outward from the electrode surface: (i) tissue coagulation, (ii) cellular edema/necrosis, (iii) sinusoidal stasis, (iv) parenchymal shunting, and (v) normal liver tissue. Reversal of stasis in sinusoids and small (<25 microm) vessels occurred at tip temperatures below 50 degrees C. This zone of stasis corresponded to the hyperemic zone on histologic analysis. Although alterations in permeability and phagocytic activity were first identified at 43 degrees C, tip temperatures higher than 55 degrees C always produced local endothelial leakiness to carbon microparticles at the periphery and always inhibited phagocytic activity. At tip temperatures higher than 95 degrees C, microbubble formation occurred with bubbles ultimately tracking through necrotic tissue into patent sinusoids. Larger peripheral vessels (>30 microm) limited extension of coagulation. CONCLUSION: Although coagulation occurs at tip temperatures higher than 50 degrees C, RF heating induced reversible microvascular stasis at temperatures lower than 50 degrees C. Increased sinusoidal endothelial permeability occurs at near-coagulative temperatures. Therefore, targeted endovascular microparticle delivery through this leaky endothelium may provide an additional and complimentary adjunct for RF ablation therapy.

Animals↗

PubMedDate not supplied

Halothane-induced intrahepatic portovenous shunting reduces hepatic microvascular sinusoidal perfusion during contrast angiographic procedures.

PURPOSE: Reduced intrahepatic perfusion that occurs during contrast angiography performed after administration of halothane anesthesia is thought to result from halothane-induced systemic hemodynamic alterations, such as reduced splanchnic blood flow, rather than intrahepatic microvascular alterations. The authors postulate that intrinsic hepatic effects caused by inhalational anesthetic agents rather than contrast materials, further reduce liver perfusion. MATERIALS AND METHODS: With use of dynamic video microscopy, intrahepatic microvascular flow rates and patterns, hepatic cord/sinusoidal diameters, portal venous pressure changes, and quantitative and qualitative Kupffer cell phagocytic activity were continuously recorded in isolated perfused rat livers before and during exposure to 1.5% halothane in O2/CO2, with and without the addition of iothalamate meglumine. RESULTS: Exposure of livers to halothane resulted in intrahepatic portovenous shunting secondary to obstruction to sinusoidal outflow, diminished sinusoidal perfusion, and a mean elevation in terminal portal venous pressure of 12.8 mm Hg. Kupffer cell phagocytic activity was reduced even when normalized for flow within sinusoids. None of these changes were attributed to use of contrast material. CONCLUSIONS: Alterations in hepatic blood flow during exposure to halothane result, in part, from increased intrinsic hepatic vascular resistance, sinusoidal outflow obstruction, and portovenous shunting, and not only from systemic hemodynamic changes. Iothalamate meglumine produced no microvascular alterations.

Anesthetics, Inhalation↗

PubMed2003

Calphostin C as a rapid and strong inducer of apoptosis in human coronary artery smooth muscle cells.

Vascular smooth muscle cells (VSMCs) play a major role in the development of atherosclerotic and restenotic lesions. The apoptotic process has been implicated in the development of this pathology. In this study, we characterized the induction of apoptosis by calphostin C (CC), a protein kinase C (PKC) inhibitor, in primary human coronary artery smooth muscle cells in the presence and absence of insulin-like growth factor-I (IGF-I). Additionally, we investigated the signal transduction pathways important for IGF-I mediated protection. Calphostin C induced apoptosis, as measured by terminal deoxy-UTP nick-end labeling (TUNEL), in a time- and dose-dependent manner, approaching 20% within 6 h of 50 nM calphostin C treatment. The amount of apoptosis increased to 44.58+/-8.08%, 47.54+/-1.66% and 78.1+/-11.9% after 8, 10 and 12 h of treatment, respectively (p<0.01 vs. control). IGF-I offered significant protection (p<0.05) at 8 and 10 h of treatment (60.6% and 52.5% protection, respectively). DNA ELISA confirmed the apoptotic effect of calphostin C and the protective effect of IGF-I. After 6 h of calphostin C treatment, DNA ELISA revealed 11.20+/-1.53 fold greater apoptosis as compared to baseline values. IGF-I treatment offered a level of protection of 46.6% as measured by DNA ELISA (p=0.06). Apoptosis was further qualitatively confirmed by time-lapse video microscopy and scanning electron microscopy. Interestingly, inhibitors of phosphatidylinositol-3-kinase (PI-3-K), p38 and extracellular regulated kinase (ERK) activation significantly (p<0.05 vs. calphostin C only treatment) increased apoptosis when used in conjunction with calphostin C. Inhibitors of phospatidylinositol-3-kinase and ERK activation reversed IGF-I protection. However, the p38 inhibitor SB203580 failed to reverse IGF-I protection. This study characterized an apoptotic system for human coronary artery smooth muscle cells offering a rapid and strong induction of programmed cell death (PCD) that remains responsive to the survival effects of IGF-I. Studies utilizing this system may prove useful in understanding the apoptotic response of VSMCs in the arterial wall.

Androstadienes↗

PubMed1995

DNA conformational dynamics in polymer solutions above and below the entanglement limit.

Video microscopy of nucleic acids (DNA) undergoing electrophoresis in hydroxyethyl cellulose (HEC) sieving buffers demonstrates previously unobserved shape-changing interactions between DNA and HEC molecules. We provide the first visual demonstration of entanglement between DNA and one or several discrete HEC molecules, which has been postulated to occur in ultradilute polymer solutions. Typically, nucleic acids appear to become entangled with HEC at a single region only, in both dilute and fully entangled HEC solutions. Fluctuations of the center of mass velocity of a DNA molecule and its correlation with conformation are revealed from analyses of the image data. These observations account for the success of recently reported rapid, high-resolution dc and pulsed-field capillary electrophoretic separations of nucleic acids in ultradilute hydroxyethyl cellulose solutions and hydroxyethyl cellulose/poly(ethylene oxide) solutions.

Cellulose↗

PubMed1995

Kinetic stabilization of microtubule dynamics at steady state in vitro by substoichiometric concentrations of tubulin-colchicine complex.

We have analyzed the effects of tubulin-colchicine (TC)-complex on the dynamic instability behavior of bovine brain microtubules at steady state in vitro using video microscopy. Incorporation of low numbers of TC-complexes per microtubule strongly suppressed dynamics at the plus ends by reducing the rate and extent of growing and shortening and by increasing the time microtubules spent in an attenuated state, neither growing nor shortening detectably. In addition, TC-complex strongly suppressed the catastrophe frequency and increased the rescue frequency. At low concentrations (0.02-0.05 microM), TC-complex suppressed dynamics without reducing the polymer mass or the mean microtubule length. Such strong suppression of microtubule dynamics by low TC-complex concentrations in the absence of polymer mass changes demonstrates that microtubule dynamics are more sensitive to the actions of TC-complex than the polymer mass. Significant reduction of polymer mass occurred at relatively high TC-complex concentration (> 0.05 microM). However, the surviving microtubules were extremely stable. Thus, TC-complex stabilizes microtubules even though the microtubules can transiently depolymerize when TC-complex is added. The data also directly establish that kinetic suppression of dynamics by colchicine at low concentrations is effected by a low number of TC-complexes at the microtubule ends.

Animals↗

PubMed1997

Mechanism of action of the unusually potent microtubule inhibitor cryptophycin 1.

Cryptophycin 1 is a remarkably potent antiproliferative compound that shows excellent antitumor activity against mammary, colon, and pancreatic adenocarcinomas in mouse xenographs. At picomolar concentrations, cryptophycin 1 blocks cells in the G2/M phase of the cell cycle by an apparent action on microtubules. The compound binds to tubulin, inhibits microtubule polymerization, and depolymerizes preformed microtubules in vitro. Its exceptionally powerful antitumor activity (many-fold greater than paclitaxel or the vinca alkaloids) raises important questions about its mechanism of action. By quantitative video microscopy, we examined the effects of cryptophycin 1 on the dynamics of individual microtubules assembled to steady state from bovine brain tubulin. At low nanomolar concentrations, in the absence of net microtubule depolymerization, cryptophycin 1 potently stabilized microtubule dynamics. It reduced the rate and extent of microtubule shortening and growing and increased the frequency of rescue. The results suggest that cryptophycin 1 exerts its antiproliferative and antimitotic activity by binding reversibly and with high affinity to the ends of microtubules, perhaps in the form of a tubulin-cryptophycin 1 complex, resulting in the most potent suppression of microtubule dynamics yet described.

Animals↗

PubMed2005

Droplet evaporation study applied to DNA chip manufacturing.

DNA chips are potentially powerful technologies for genotyping and gene expression profiling that rely on comparative analyses of up to thousands of "spots of analysis" on a glass support. The spot quality throughout the support influences spot-to-spot variations within an array and the repeatability of data across experiments. For glass slide DNA microarrays, droplets of DNA solution are deposited on functionalized glass slides and left to react through complete evaporation of the droplet. On hydrophobic flat surfaces, different modes of droplet evaporation can be attained. Under atmospheric pressure, water droplets tend to evaporate under two main regimes. Initially, the droplet flattens with a constant contact area, and then the droplet shrinks at a constant contact angle. As a result, the diameter and morphology of thousands of spots on microarrays are not uniform. This leads to poor and unreliable data processing results. In this work, we report the evaporation of an aqueous solution under a constant contact area mode. Evaporation under reduced pressure and the effect of reagent additives to the solution have been investigated. Video microscopy and digital image analysis techniques were applied to monitor the evaporation of the droplets. A mixture of surfactants was developed to maintain a constant area regime during evaporation and to form homogeneous spots. The control of some physicochemical properties (wetting, evaporation rate) of the droplet allows the formation of well-controlled spots compatible with DNA grafting. The influence of surfactant molecules on the mechanisms of evaporation is also discussed.

Atmospheric Pressure↗

PubMed2002

Effects of the inhibitors of dynamics of cytoskeletal structures on the development of apoptosis induced by the tumor necrosis factor.

Changes in cytoskeletal structures have been investigated during apoptosis of epithelial HeLa cells induced by tumor necrosis factor-alpha (TNF-alpha). Shape and surface cell activity were investigated by time-lapse video microscopy, and changes of the cytoskeletal structure were studied by immune fluorescent microscopy. Addition of TNF-alpha to HeLa cell culture caused early disruption of the actin cytoskeleton and vinculin-containing focal contacts, keratin filaments, and microtubules. Rounding of cells, general blebbing, and nuclear fragmentation were observed at the terminal apoptotic stages. Actomyosin complex inhibitors, H7 and HA1077, suppressed blebbing (but not cell rounding) and activated the development of apoptosis. The latter suggests that in contrast to blebbing the general rounding does not depend on increased contractility of actomyosin cortex. These cytoskeletal inhibitors accelerated the development of apoptosis of HeLa cells and increased sensitivity of HeLa-Bcl-2 cells (transfected with DNA encoding antiapoptotic protein Bcl-2) to TNF-induced apoptosis. Damage of cytoskeletal structures significantly attenuated antiapoptotic activity of Bcl-2 in the HeLa-Bcl-2 cells. It is suggested that the stimulation of apoptosis by cytoskeletal inhibitors may be attributed to the altered distribution of cell organelles, especially, mitochondria.

Actomyosin↗