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R L Schultz

Publications and source records attributed to R L Schultz.

At least 19 recordsLinked to original sources
PubMed1992

Lipoproteins enhance fibronectin binding to adherent cells.

We have identified very low density (VLDL) and low density (LDL) lipoproteins as blood plasma components that enhance the binding and deposition of fibronectin into the extracellular matrices of cultured MG-63 osteosarcoma cells and human fibroblasts. The lipoproteins increased the binding and deposition of iodinated fibronectin by MG-63 cells threefold over control levels. LDL also increased the deposition of multimeric fibronectin into extracellular matrix as assessed by gel electrophoresis and fluorescence microscopy. High density lipoprotein (HDL) and the d > 1.21 g/ml nonlipoprotein fraction had less activity. Enhancement of binding of fibronectin was observed within 15 minutes, when binding was largely reversible. LDL also increased the binding of a fragment containing the 70-kd amino-terminal region of fibronectin that is primarily responsible for the reversible binding of fibronectin to cell layers. LDL had to be present simultaneously with radiolabeled fibronectin to exert an effect on fibronectin binding. LDL enhanced fibronectin binding equally well to normal skin fibroblasts and to familial hypercholesterolemic fibroblasts lacking the LDL receptor. Acetylation of LDL, performed to block its interaction with the LDL receptor, did not diminish the enhancement of fibronectin binding to MG-63 cells. These results indicate that LDL and VLDL interact with fibronectin to potentiate binding to monolayer cells through a pathway that does not involve the LDL receptor.

Amino Acid Sequence↗
PubMed1992

Temporary cerebral ischemia. Effects of pentastarch or albumin on reperfusion injury.

Recent investigations have proposed that, after temporary ischemia, pentastarch may reduce microvascular permeability and reperfusion injury. However, this hypothesis has not been tested in the brain. Accordingly, after 180 min of temporary middle cerebral artery occlusion, the effect of pentastarch or albumin on blood-brain barrier permeability and cerebral injury was investigated in isoflurane-anesthetized rats. One of the following was maintained for the final 60 min of occlusion and throughout reperfusion: control-hematocrit was not manipulated; pentastarch-hematocrit was decreased to approximately 30% with pentastarch; or albumin-hematocrit was decreased (approximately 30%) with albumin. Part A (n = 21): 30 min of reperfusion was allowed, and blood-brain barrier permeability was determined with the indicator dye Evans Blue. Part B (n = 14): in different animals, 120 min of reperfusion was allowed, and cerebral injury (2,3,5-triphenyltetrazolium chloride stain) and edema (specific gravity) were assessed. Part C (n = 4): in different animals, the blood-brain barrier was evaluated by electron microscopy. Evans Blue (micrograms per gram brain tissue, mean +/- SD) was greater in the control (20.8 +/- 9.0) and albumin (15.5 +/- 7.3) groups versus the pentastarch (4.7 +/- 2.7) group (P less than 0.05). Brain injury (percent of hemisphere ipsilateral to occlusion) was less and specific gravity greater in the pentastarch (33 +/- 8 and 1.040 +/- 0.003 respectively) versus the albumin group (45 +/- 6 and 1.035 +/- 0.003). This study supports the hypothesis that during temporary cerebral ischemia, pentastarch decreases brain injury and edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1991

Time- and pressure-dependent changes in blood-brain barrier permeability after temporary middle cerebral artery occlusion in rats.

After 180 min of temporary middle cerebral artery occlusion in rats, the affect of phenylephrine-induced hypertension on blood-brain barrier permeability was assessed. One of the following blood-pressure regimens was maintained during either a 30- or 120-min period of reperfusion: (a) 30/Norm, 30 min of normotensive reperfusion was allowed; (b) 30/HTN, mean arterial blood pressure was increased by 35 mm Hg during 30 min of reperfusion; (c) 120/Norm, 120 min of normotensive reperfusion was allowed; or (d) 120/HTN, mean arterial blood pressure was increased by 35 mm Hg during 120 min of reperfusion. Evans blue (30 mg/kg) was given, and brains were analyzed for Evans blue by spectrophotometry. Evans blue (microgram/g brain tissue, mean +/- SD) was greater (P less than 0.05) in both hypertensive groups versus their time matched normotensive groups (30/HTN: 80 +/- 16 versus 18 +/- 6 in the 30/Norm group; 120/HTN: 17 +/- 6 versus 8 +/- 3 in the 120/Norm group). In addition, Evans blue was greater (P less than 0.05) in both 30-min groups versus their pressure matched 120-min groups (30/Norm: 18 +/- 6 versus 8 +/- 3 in the 120/Norm group; 30/HTN: 80 +/- 16 versus 17 +/- 6 in the 120/HTN group). The data are consistent with previous studies which have demonstrated an opening of the blood-brain barrier at the onset of reperfusion. In addition, the data support a hypothesis that changes in blood-brain barrier permeability are more sensitive to hypertension in the early period of reperfusion.

Animals↗
PubMed1990

Prenatal development of "synaptic" ribbons in the guinea pig pineal gland.

Pineal "synaptic" ribbons are a heterogeneous population of organelles. "Synaptic" ribbons (SR) sensu stricto, "synaptic" spherules (SS), and intermediate forms (IMF) are present. Their function and origin are unknown, and a knowledge of their prenatal development is lacking. Thus the pineal glands of prenatal, neonatal, and adult guinea pigs were prepared for electron microscopy. "Synaptic" ribbons were studied morphologically and quantitatively. The three categories of "synaptic" ribbons reported in adult pineal glands were also present in prenatal pineal glands. Their structural features, distribution, grouping, and composition patterns are similar to those in adults. "Synaptic" ribbons were first detected in pinealocytes of the distal region of a 42-day postcoitus (PC) pineal gland and were comparable with those in adults. They increased in number with age and reached a peak at 63 days PC, followed by a steep decline at 66 and 67 days PC. By day 69 PC, the numbers increased again and showed a dramatic increase after birth. Several true ribbon synapses were seen at day 63 PC between pinealocyte cell processes or between pinealocyte cell process and pinealocyte cell body. Since true ribbon synapses have not been found in adult guinea pig pinealocytes, their synaptic nature could have been lost during development. No precursors for the "synaptic" ribbons were found. The endoplasmic reticulum cisternae may be the origin for the ribbon vesicles because of their close association with the "synaptic" ribbons.

Aging↗
PubMed1990

Ultrastructural localization of acetylcholinesterase in the guinea pig pineal gland.

The ultrastructural localization of acetylcholinesterase (AChE) activity in guinea pig pineal gland was studied using the copper-glycine procedure. A small number of pinealocytes and bundles of unmyelinated nerve fibers were labeled by the AChE reaction. The AChE-positive pinealocytes were located near blood vessels and distributed in small groups. The AChE reaction product was localized in the perinuclear cistern, in the cisternae of the endoplasmic reticulum (ER), and in the saccules of the Golgi apparatus. These findings suggest that the AChE-positive pinealocytes synthesize AChE. The AChE reaction product was also seen in the intercellular space between pinealocyte processes. Besides pinealocytes, AChE activity was localized on the axolemma of myelinated and unmyelinated nerve fibers and in the basement membrane surrounding unmyelinated nerve fibers. Pseudocholinesterase activity was confined to Schwann cells, which showed the reaction product in their perinuclear cistern, in the cisternae of the ER, and on the plasmalemma.

Acetylcholinesterase↗
PubMed1990

Ultrastructural localization of phosphatase activity in the guinea pig pineal gland by the cerium technique.

Thiamine pyrophosphatase (TPPase), nucleoside diphosphatase (NDPase), and glucose-6-phosphatase (G-6-Pase) were localized by the cerium technique in guinea pig pinealocytes and compared with the corresponding lead technique. NDPase and TPPase were also compared at different pH values using the cerium technique. Vibratome sections of perfusion-fixed tissue were incubated with cerium chloride or lead nitrate. Substrates used were thiamine pyrophosphate (for TPPase), sodium inosine diphosphate (NDPase), and disodium glucose-6-phosphate (G-6-Pase). The 1-2 trans saccules of the Golgi apparatus showed TPPase and NDPase activity but none for G-6-Pase. The endoplasmic reticulum (ER) cisternae and perinuclear space had NDPase and G-6-Pase activity but not TPPase. The abluminal plasmalemma of endothelial cells and the plasmalemma of Schwann cells demonstrated TPPase and NDPase activity but the luminal plasmalemma of the endothelial cells and the plasmalemma of pinealocyte processes showed only NDPase activity. TPPase was active at all pH values tested, but NDPase was most active at pH values of 6.5 and 7.0. Lead phosphate precipitate was frequently seen in nuclei, perinuclear space, ER cisternae, and "synaptic" vesicles when lead was used as the capturing agent. These sites were usually not labeled when cerium was used.

Acid Anhydride Hydrolases↗
PubMed1989

Rapid changes of light microscopic indices of osteoclast-bone relationships correlated with electron microscopy.

The relationships of tibial endosteal osteoclasts to bone surfaces were quantitatively evaluated during initiation of calcium repletion in calcium-deficient rats. To do this, indices of osteoclast-bone relationships obtained by light microscopy were devised and evaluated by comparing with those obtained by electron microscopy (EM). These indices are the percent of the osteoclast width that (1) exhibits markers indicative of a ruffled border, (2) is in close contact with bone, (3) is isolated from bone by other cell types, and (4) is separated from bone by intercellular material. The indices obtained by light microscopy were strongly correlated with similar indices obtained by EM and were equally sensitive but considerably easier to obtain. The ruffled border and contact index were significantly decreased by 3 hours after beginning the meal whereas cells of other types became interposed between the osteoclasts and the bone.

Animals↗
PubMed1989

Improved procedures for pineal gland fixation for electron microscopy.

The common procedures used for preparing some organs and tissues for electron microscopy, in which a fixative with the buffer portion adjusted to near-isotonicity to plasma is perfused in vivo, causes intolerable shrinkage of rat pineal cells. The present study was undertaken to optimize the parameters involved in the fixation of the pineal gland. The buffer and its concentration and the aldehyde or aldehydes used were among the variables investigated. The buffers tried were phosphate, cacodylate, PIPES, and HEPES. Decreasing the buffer concentration prevented shrinkage with all four buffers. The optimum concentrations were 0.05 M phosphate, 0.07 M cacodylate, 0.05 M or 0.057 M PIPES, and 0.1 M HEPES. PIPES and HEPES were clearly superior in retaining cytoplasmic density when compared with phosphate or cacodylate. The use of lithium PIPES and HEPES instead of the sodium equivalents enhanced membrane detail. A small volume of more concentrated aldehyde fixative perfused ahead of the main perfusate (a strong prewash) definitely helped prevent shrinkage. Using a mixture of aldehydes consisting of glutaraldehyde, formaldehyde, and acrolein reduced the tendency for shrinkage when compared with glutaraldehyde only. Some of the shrinkage space artefacts could be easily misinterpreted as normal features. Since the pineal gland commonly contains degenerating structures, a dependable fixation procedure is particularly needed. Also, accurate preservation is essential in the evaluation of physiological changes.

Animals↗
PubMed1988

Plasma vitronectin polymorphism in normal subjects and patients with disseminated intravascular coagulation.

Vitronectin, also known as serum-spreading factor or S-protein, mediates cell adhesion and inhibits formation of the membrane-lytic complex of complement and the rapid inactivation of thrombin by antithrombin III in the presence of heparin. Vitronectin is normally present in plasma at a concentration of approximately 300 micrograms/mL. The investigators quantified plasma vitronectin with an enzyme-linked immunosorbent assay and visualized reduced and nonreduced vitronectin by immunoblotting after separation of plasma or serum by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The concentration of plasma vitronectin was markedly reduced in some patients with disseminated intravascular coagulation, especially in those with liver failure; it was near normal in patients with metastatic cancer and acute leukemia. Patients with vitronectin levels less than 40% normal invariably had low fibrinogen and antithrombin III and a prolonged prothrombin time. In both normal and patient plasmas there was heterogeneity in the ratio of the 75,000- and 65,000-mol wt polypeptides of reduced vitronectin: 18% had mostly the 75,000-mol wt polypeptide, 59% had roughly equal amounts of the two polypeptides, and 22% had mostly the 65,000-mol wt polypeptide. This polymorphism is inherited and appears to be due to two alleles that are present with approximately equal frequency. The blotting patterns of vitronectin in reduced and nonreduced plasmas were largely unaltered in plasma of patients with defibrination syndrome, fibrinolysis, liver failure, sepsis, metastatic cancer, and acute leukemia. There was no evidence of fragmentation of vitronectin or formation of the disulfide-bonded complex of vitronectin and thrombin-antithrombin III that is found when blood is clotted. Thus these results corroborate in vitro observations that the liver is the major source of plasma vitronectin, suggest that vitronectin may become depleted during disseminated intravascular coagulation, and define a genetic polymorphism of vitronectin.

Animals↗
PubMed1986

Membrane alterations in cerebral cortex when using PIPES buffer.

When used for vascular perfusion of brain, 0.1 M PIPES-buffered 3% glutaraldehyde resulted in the formation of expanded, vesicle-filled cell processes limited by multiple membrane layers. These structures, termed multivesicular myelin figures and interpreted as artefacts, were most common in layer 2 of the cerebral cortex. When cacodylate or phosphate buffer was used instead of PIPES buffer in the primary fixative, such structures were not seen. The use of a more concentrated initial aldehyde fixative, PIPES-buffered, markedly reduced the size and numbers of these artefacts when compared to PIPES-buffered 3% glutaraldehyde only. Slowing the initial perfusion rate increased the size and frequency of occurrence of multivesicular myelin figures with PIPES buffer when compared to optimum perfusions. Prolonged initial exposure to PIPES buffer by using it to wash out the blood and then perfusing with fixative 5 min later did not increase the number or size of multivesicular myelin figures but did reduce the multivesicular nature of the artefacts. We suggest that the non-toxic nature of PIPES buffer allowed the formation of these membranous artefacts, while phosphate and cacodylate interfered with the cellular activity during the process of fixation.

Alkanesulfonates↗
PubMed1978

The origin of lipofuscin and possible consequences to the myocardium.

Examination by light and electron microscopy of human myocardium from necropsies and biopsy specimens has revealed evidence that mitochondria can be transformed into granules of lipofuscin. This pigment has been shown to arise from peroxidative destruction of polyunsaturated lipid membranes. A high rate of lipofuscin formation is indicated by the occurrence of brown atrophy of the heart in relatively young persons who died of conditions that were associated with inanition. Such lipofuscin formation suggests the importance of dietary antioxidants in preventing peroxidative damage to mitochondria. A by-product of lipid peroxidation, malonaldehyde, can react with nuclear DNA, blocking template activity. Nuclear damage of this kind could reduce the capacity for protein synthesis and limit mitochondrial and contractile protein replacement. Such a limitation would contribute to heart failure during stress. Peroxidative damage to the myocardium is cumulative and irreversible.

Adult↗
PubMed1976

The ultrastructure of the sheath around chronically implanted electrodes in brain.

Insulated, bipolar stainless steel electrodes were chronically implanted in various regions of the cat brain and the long-term structural changes in the tissue surrounding the electrodes were studied by light and electron microscopy. A sheath surrounded and separated the electrode from normal grey or white matter. A layer of foreign body giant cells of variable thickness was formed adjacent to the electrode. This layer was attenuated in some places so that it was unrecognizable by light microscopy. The bulk of the sheath structure consisted of collagen fibrils, leptomeningeal cells and hypertrophied astrocytes. Areas consisting of modified leptomeningeal cells with long thin processes we designated as spongy areas. These have not been previously reported using the electron microscope. Glycogen bodies were seen in leptomeningeal cells. Astrocytes became greatly enlarged and were more numerous in and around the sheath. Oligodendrocytes contained lamellar bodies, and direct continuity was shown between a lamellar body and an adjacent myelin sheath. Myelin was seen in abnormal sites (around oligodendrocytes and neurons) and in unusual configurations. Neuronal changes near the sheath included whorls and stacks of modified endoplasmic reticulum and the presence of cytoplasmic nucleolus-like bodies. Reactive, regenerative and degenerative axons were observed. Blood vessels were more numerous in the sheath and surrounding tissue than normal. Perivascular spaces were prominent even around capillaries and often plasma cells and monocytes were in these spaces. As compared to normal tissue the extracellular space is noticeably increased. Electrodes passing through ventricles were surrounded with a sheath covered with ependymal cells. This sheath was comparable in structure to the sheath present around the electrode in other locations.

Animals↗
PubMed1975

Cation-dependent structures associated with membranes in the rat central nervous system.

As observed by high magnification electron microscopy, potassium ions induce osmiophilia at the extracellular side of triple layered plasma membranes in the central nervous system of the rat. In contrast, sodium ions induce a widening of the intracellular lamina of these membranes, and do not result in observable extracellular deposits. The observations suggest the existence of potassium and sodium ion-selective structures associated with opposite surfaces of the neuron membrane. Use of the fixative vehicle as a cytochemical reagent is proposed.

Animals↗