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J M Rodenburg

Publications and source records attributed to J M Rodenburg.

12 recordsLinked to original sources

Transmission microscopy without lenses for objects of unlimited size.

We demonstrate experimentally, for the first time, a new form of lensless microscopy. The image we obtain contains the entire wavefunction emanating from the sample. Large scale, quantitative phase information can be measured, unlike in conventional (Zernike) methods. For light optical experiments, we can dispense with expensive high-quality lenses and the very large working distances available would allow remote monitoring of e.g., environmental cells without compromising resolution. In short wavelength microscopy (X-rays and electrons), where lens components are of very limited numerical aperture, the technique has revolutionary implications: objects of any lateral size or shape can be used and, for transmission electron imaging, resolution down to the scale of the wavelength is likely to be limited only by the presence of atomic vibrations.

Journal Article↗

Error tolerance of an iterative phase retrieval algorithm for moveable illumination microscopy.

This paper examines the behaviour of the new Ptychographical Iterative Engine (PIE) algorithm when part of the initial information it requires is inaccurately known. This could be the parameters describing the illuminating wavefunction, the precise location of the specimen relative to the illuminating wavefunction, or other information that is assumed about the physical system. The tolerance of the algorithm for unavoidable problems such as noise and source incoherence is also investigated, leading to the conclusion that this approach to phase retrieval is very robust. It can not only tolerate errors in the assumed parameters, but can often be used as a method of characterising the parameters more accurately.

Journal Article↗

Movable aperture lensless transmission microscopy: a novel phase retrieval algorithm.

We propose an iterative phase retrieval method that uses a series of diffraction patterns, measured only in intensity, to solve for both amplitude and phase of the image wave function over a wide field of view and at wavelength-limited resolution. The new technique requires an aperture that is scanned to two or more positions over the object wave function. A simple implementation of the method is modeled and demonstrated, showing how the algorithm uses overlapping data in real space to resolve ambiguities in the solution. The technique opens up the possibility of practical transmission lensless microscopy at subatomic resolution using electrons, x rays, or nuclear particles.

Journal Article↗

A simple model of holography and some enhanced resolution methods in electron microscopy.

A simple pictorial model of electron interference effects based on an extended representation of the autocorrelation function is described and developed. Unlike Abbe's theory of transmission imaging, the model incorporates fully the effect of the loss of phase that occurs in the detector plane. The aperture transfer function and information limit (envelope function) are also incorporated with reference to the simplest scattering geometry of Young's slits. The model is then applied to holography, the diffraction phase problem, ptychography, Wigner distribution deconvolution, conventional bright-field imaging, single side-band imaging and tilt-series reconstruction. Some of these methods require an understanding of four-dimensional integral functions, but the model reduces the problem into a projection of a two-dimensional space. It is hoped that the model will help material scientists who are not specialists in imaging and diffraction theory to understand some recent developments in advanced super-resolution imaging methods.

Image Processing, Computer-Assisted↗

Effects of Hoe-140 and ramiprilat on arteriolar tone and dilation to bradykinin in skeletal muscle of rats.

In skeletal muscle of pentobarbital sodium-anesthetized rats, the mechanism of action and possible role of the potent vasodilator bradykinin (BK) in regulation of arteriolar tone were investigated. Changes in diameter of third-order arterioles of cremaster muscle in response to topical administration of BK and other vasoactive agents were measured with an image-shearing monitor and recorded with video microscopy. All agonists were administered topically on the exteriorized muscle. With use of Hoe-140, a B2-receptor antagonist, the presence of kinin receptors in arterioles was studied. In control preparations, 10(-5) M arachidonic acid (AA), 0.5 x 10(-6) M acetylcholine (ACh), and 10(-5) M adenosine (ADO) evoked dilation of arterioles of up to 70% of resting diameter. BK (10(-9), 10(-8), 10(-7), and 10(-6) M) elicited dose-dependent arteriolar dilations (1.3 +/- 1.3, 4.1 +/- 0.5, 10.3 +/- 1.6, and 13.3 +/- 1.3 microns, respectively). In the presence of 10(-7) M Hoe-140, dilations to AA, ACh, and ADO were not affected, but those to 10(-9)-10(-7) M BK were eliminated or significantly inhibited (10(-6) M BK: to 2.9 +/- 1.8 microns). Also, whereas Hoe-140 significantly reduced basal arteriolar diameters (from 16.7 +/- 0.9 to 13.8 +/- 1.1 microns, P < 0.05), it did not affect constrictions to norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗

Regulation of arteriolar tone and responses via L-arginine pathway in skeletal muscle.

With in vivo television microscopy, changes in arteriolar diameter to topical administration of various vasoactive agents were examined in the absence or in the presence of NG-monomethyl-L-arginine (L-NMMA, topical 100 microM) or NG-nitro-L-arginine (L-NNA, 2.5 microM, 20 microliters/min ia), specific inhibitors of endothelium-derived relaxing factor (EDRF) biosynthesis. In cremaster muscle arterioles (15-22 microns) of rats (n = 6-11), dilations to acetylcholine (1-100 ng) were significantly inhibited (60-70%) by either of the arginine analogues. This inhibition was reversed by subsequent administration of 1 mM L-arginine. Dose-dependent constriction to norepinephrine was enhanced by L-NMMA. Indomethacin treatment reduced arteriolar dilation to bradykinin (BK, 1-100 ng), which was significantly inhibited by additional administration of L-NNA. Application of L-NNA first, followed by additional indomethacin, elicited similar results. Dilations to sodium nitroprusside and adenosine were not reduced in the presence of the inhibitors. L-NMMA or L-NNA caused no change in systemic blood pressure but elicited a significant reduction in arteriolar diameter; this effect was not reversed by 1 mM L-arginine. These data demonstrate the presence of an L-arginine pathway to produce EDRF (nitric oxide) in skeletal muscle microcirculation that mediates and/or modulates arteriolar responses to vasoactive agents and could contribute to the regulation of basal vascular tone.

Animals↗

Modified arteriolar responses to ATP after impairment of endothelium by light-dye techniques in vivo.

In this study we investigated whether endothelial cells are involved in the dilation of third-order arterioles (14 to 22 microns) in response to adenosine triphosphate (ATP) in cremaster muscle of pentobarbital-anesthetized rats. Two light/dye (L/D) techniques were employed to achieve selective, local endothelial impairment. One of these techniques utilizes a mercury lamp and sodium fluorescein, the other a Helium-Neon laser and Evans blue dye. L/D treatment (illumination with the appropriate wavelengths of light in the presence of an intravascular dye) of a 20-to 100-microns segment of an arteriole resulted in a complete loss of arteriolar dilation in response to topical administration of acetylcholine (10(-6) M) and arachidonic acid (AA, 10(-5) M). These agents were applied in 100-microl aliquots without interrupting the continuous suffusion with Ringer-gelatin solution and caused a approximately 70% increase in vascular diameter before the L/D intervention. Selectivity of the impairment was assessed by arteriolar responses to the nonendothelium-dependent dilator agents adenosine (10(-5) M) and sodium nitroprusside (2 X 10(-7) M), which elicited the same degree of dilation before and after L/D treatment. Under control conditions ATP (10(-6), 10(-5), and 10(-4) M) elicited dose-dependent increases in arteriolar diameter (from 38 to 74%). After impairment of arteriolar endothelium, dilation in response to all doses of ATP was significantly reduced. Theophylline (30 microM) significantly inhibited arteriolar dilation in response to adenosine (10(-6), 10(-5), and 10(-4) M) but did not affect the responses to various doses of ATP. Moreover, impairment of endothelium enhanced constrictor responses of arterioles to norepinephrine (0.6 X 10(-8) M). These results indicate that arteriolar endothelium of skeletal muscle can mediate or modulate arteriolar responses to various vasoactive agents, suggesting that it has an important role in the regulation of blood flow.

Acetylcholine↗

Methylene blue inhibits vasodilation of skeletal muscle arterioles to acetylcholine and nitric oxide via the extracellular generation of superoxide anion.

The mechanism of modulation of cyclic GMP-associated vascular responses by methylene blue, an agent employed to inhibit the activation of soluble guanylate cyclase in tissues, was investigated in the cremaster muscle microcirculation of pentobarbital-anesthetized rats. The effect of topically applied agents on the diameter of third-order arterioles (15-20 microns diameter) was determined by in vivo television microscopy. Topical application (100 microliters) of acetylcholine (0.01 microgram) or nitric oxide (0.06-6 micrograms) caused vasodilator responses that were inhibited (P less than .05, n = 6-8) 64% and 30 to 100%, respectively, by suffusion of the preparation with 5 microM methylene blue. Agents that are thought to produce activation of guanylate cyclase via cellular metabolism to nitric oxide, nitroglycerin (0.5 ng-0.5 microgram) or nitroprusside (0.5 ng-0.5 microgram), also produced vasodilation. However, methylene blue suffusion did not inhibit these responses (n = 6-9). The inhibition of vasodilation to acetylcholine or nitric oxide by methylene blue was completely prevented by suffusion of superoxide dismutase, but not affected by suffusion of catalase. Based on the current conceptualization of the mechanism of action of these vasodilator agents in isolated larger blood vessels, methylene blue appears to inhibit responses in this skeletal muscle microcirculatory preparation through the extracellular generation of superoxide anion and not via a direct interaction with guanylate cyclase.

Acetylcholine↗

Similarities in the pharmacological modulation of reactive hyperemia and vasodilation to hydrogen peroxide in rat skeletal muscle arterioles: effects of probes for endothelium-derived mediators.

Our laboratory has demonstrated previously that prostaglandins are partially responsible for the vasodilation of rat cremaster muscle arterioles in vivo to a brief occlusion or hydrogen peroxide (H2O2). In the present study, in pentobarbital-anesthetized rats, we investigated the mechanism of the prostaglandin-independent portion of the dilation to these stimuli by measurement of changes in the diameter of third order cremasteric arterioles (approximately 15 microns) by video microscopy. In the presence of indomethacin suffusion (10 micrograms/ml), arteriolar dilation to the release of a 15-sec occlusion of a single arteriole or to topical application of 0.1 to 1 mM H2O2 (100 microliters) was reduced significantly by suffusion of 20 microM quinacrine or 5 microM methylene blue, whereas vasodilation to adenosine was not affected by these probes. Furthermore, the reactive hyperemia was not altered by suffusion of 50 microM hydroquinone or 0.2 mM NG-monomethyl-L-arginine, inhibitors of the dilation to acetylcholine mediated by the endothelium-derived relaxing factor. Reactive hyperemia was also not affected by 30 microM theophylline (an adenosine antagonist) or suffusion of catalase (160 U/ml) plus superoxide dismutase (240 U/ml). Therefore, the reactive hyperemia does not appear to be mediated through endothelium-derived relaxing factor, adenosine or the extracellular formation of reactive O2 species. However, these observations suggest that the prostaglandin-independent vasodilation to H2O2 and to the release of a brief arteriolar occlusion may be mediated by a common mechanism, possibly involving cyclic GMP. Similarities in pharmacological modulation of the dilation after occlusion and to H2O2 in the cremaster microcirculation suggest consideration of the involvement of H2O2 in the hyperemic response.

Animals↗

Endothelium-associated vasodilators in rat skeletal muscle microcirculation.

Pharmacological probes were used to assess the possible roles of guanosine 3',5'-cyclic monophosphate (cGMP)-associated endothelium-derived relaxing factor (EDRF) in mediating microvascular responses to endogenous and exogenous agents in vivo. Pentobarbital-anesthetized rats (Wistar, 6 wk old) were prepared for in vivo microscopic observation and quantification of changes in diameter of third-order arterioles (15-25 microns) in the cremaster muscle to topical application of all agents. In indomethacin-pretreated preparations, cremasteric arteriolar dilator responses to acetylcholine, bradykinin, or ATP, but not to adenosine, histamine, or prostaglandin E2, were inhibited by hydroquinone (50 microM). Vasodilation to acetylcholine was also inhibited by methylene blue (5 microM), a blocker of guanylate cyclase activation. Constrictor responses to norepinephrine were not affected by hydroquinone or methylene blue. The inhibition of acetylcholine-induced vasodilation by hydroquinone and methylene blue was reversed by superoxide dismutase, suggesting that superoxide anion antagonized the response. On the other hand, basal arteriolar diameters or responses to acetylcholine were not affected by oxygen metabolite scavengers. Unlike in isolated arteries, vasodilator responses to the calcium ionophore A23187 or arachidonic acid were completely antagonized by cyclooxygenase inhibition. These data suggest that EDRF could be involved in the control of microvascular tone; however, significant differences exist in the stimuli that elicit dilation through this mediator in small and large blood vessels.

Acetylcholine↗

Oxygen metabolites and vasodilator mechanisms in rat cremasteric arterioles.

The effects of oxygen metabolites (superoxide anion and hydrogen peroxide) on male Wistar rat cremasteric arterioles and the involvement of these species in the mechanism of vasodilation to arachidonic acid and bradykinin were examined by in vivo television microscopy. In the present study, xanthine oxidase-derived oxygen metabolites from endogenous substrates elicited vasodilation that was selectively and almost completely inhibited by catalase but not by superoxide dismutase. These findings implicate hydrogen peroxide as the vasoactive metabolite generated. Topical application of hydrogen peroxide itself on cremasteric arterioles caused concentration-dependent dilation over the range of 10(-7) to 10(-4) M. Responses to hydrogen peroxide concentrations of up to 10(-5) M were completely inhibited by indomethacin, suggesting that hydrogen peroxide-induced increases in vessel diameter are primarily mediated through the production of vasodilator prostaglandins. In this study, we have not found any evidence to suggest that dilator responses to arachidonic acid or bradykinin are mediated through the extracellular generation of oxygen metabolites. Hydrogen peroxide-induced vasodilation might be involved in the events linking the sensing of oxygen tension through intracellular peroxide formation to the production of vasoactive mediators in the cremasteric microcirculation.

Animals↗