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Biomedical subjects

E L Hogan

Publications and source records attributed to E L Hogan.

At least 91 records · Page 5Linked to original sources
PubMed1989

Progression of hypertensive intracerebral hemorrhage.

Hypertensive intracerebral hemorrhage (HICH) is generally considered to be a monophasic event. Enlargement of the initial hematoma after several hours or days has rarely been documented. We describe the clinical and CT findings in 8 patients (5 men, 3 women, aged 39 to 68 years) with continued bleeding or rebleeding during the acute phase of HICH. The thalamus was the most frequent site of hemorrhage (6/8). The neurologic status deteriorated in all: 6 within 24 hours, and 2 after 5 and 7 days. Persistent hypertension was common (6/8) prior to extension of the hemorrhage. The 2nd CT revealed an obvious increase in hematoma size in all cases. Four patients died and 4 survived with severe neurologic disability. These serial studies indicate that active bleeding or rebleeding can occur in HICH and suggests that the risk is particularly high with thalamic hemorrhage. We conclude that meticulous control of hypertension after HICH may be justified in selected patients.

Adult↗
PubMed1988

Expression of myelin protein genes in quaking mouse brain.

The expression of myelin proteins in actively myelinating quaking and control brains was studied. RNA was extracted from the brains of 18- and 27-day-old mice and analyzed by northern blot using cDNA probes for proteolipid protein (PLP), basic protein (BP), and myelin-associated glycoprotein (MAG). Two PLP transcripts of 3.2 and 2.4 kb (kilobase) were found, whereas PB and MAG probes hybridized to single regions of 2.2 and 2.5 kb, respectively. No abnormality in the transcript pattern was detectable in the quaking brain at either 18 or 27 days of age. Over this 9-day period the level of PLP and BP message in the control brain decreased by approximately 10%, whereas the level of MAG message decreased by approximately 50%. In the 18-day-old quaking brain the expression of PLP and BP was severely reduced amounting to one-third and one-half of the control values, respectively. The reduction at the age of 27 days was less. On the other hand, the quaking brain produced more MAG mRNA amounting to 1.6- and 3.2-fold control on the 18th and 27th day. The results indicate a reduced expression of the PLP and BP genes and a developmental delay in the mutant, whereas the genetic expression of MAG is enhanced and appears to be progressively dysregulated.

Aging↗
PubMed1988

Calcium-activated neutral proteinase in rat brain myelin and subcellular fractions.

The activity of calcium-activated neutral proteinase (mM CANP) was determined in subcellular fractions of rat brain. The CANP activity in whole homogenate and its membrane fractions including myelin was increased ten-fold following treatment with Triton X-100. The majority of the activity (60%) was in the primary particulate fractions P1 (nuclear), P2 (mitochondrial), and P3 (microsomal). Following subfractionation of each particulate fraction, most of the activity (50%) was found in the myelin-enriched fractions (P1A, P2A, and P3A) and separated at the interface of 0.32-0.85 M sucrose. Only 20-30% of the total homogenate activity was in cytosol. The enrichment in the myelin fractions resembled that for 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) activity. Immunoblotting revealed that the CANP was mainly in myelin and cytosol. In addition to the presence of 72-76 Kd and 80 Kd bands, there were faint high-molecular-weight CANP bands ranging from 110-150 Kd and lower-molecular-weight forms in the region of 30-50 Kd in both purified myelin and cytosol. These studies suggested that CANP is present in myelin and cytosol and that it exists in the brain in membrane-bound and soluble forms.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1988

Glycosphingolipid biosynthesis during myogenesis of rat L6 cells in vitro.

Glycosphingolipid biosynthesis was examined using [3H]-galactose as a precursor as rat L6 myoblasts fused to form multinucleated myotubes. Incorporation of label into neutral glycolipids decreased steadily as the population of myotubes increased, so that final biosynthesis was one-half that observed with myoblasts (p less than 0.02). Conversely, ganglioside biosynthesis doubled during myoblast confluency (p less than 0.02) and then decreased as myotubes formed. Qualitatively, L6 cells synthesized large amounts of ganglioside GM3 during all myogenic phases. The major neutral glycosphingolipid products were lactosylceramide and paragloboside (nLcOse4Cer). Few changes in TLC autoradiographic patterns were noted during differentiation, with the exception of a slight decrease in ganglioside GM1. The results indicate that the biosynthesis of glycosphingolipids is tightly regulated during myogenesis in vitro and suggest a role for membrane gangliosides in muscle cell differentiation.

Animals↗
PubMed1988

Immunoglobulin G in multiple sclerosis brain.

We extracted free and bound IgG from plaques and normal-appearing white matter of multiple sclerosis (MS) brains. By isoelectric focusing (IEF), three patterns of IgG distribution were seen: (A) a restricted high-pI distribution with a specific band at low pH, (B) a restricted high-pI pattern, and (C) a broad pI pattern similar to that of the unbound IgG extracted at neutral pH. In one MS brain, we compared the IEF pattern of plaque material with that of normal-appearing white matter (NAWM); the low-pH extract of plaque material (PM) had a restricted pattern at high pI. In another MS brain, a specific band of bound IgG was found. These data suggest that MS lesions expose an antigen(s) unique to MS. B cells consequently might be stimulated by a disease-related antigen(s) in the MS lesion.

Brain↗
PubMed1988

Temporal profile of thromboxane-prostacyclin imbalance in experimental spinal cord injury.

Thromboxane-prostacyclin imbalance may be an important determinant of platelet-vessel wall interactions that are vital in circulatory homeostasis. In experimental spinal cord injury, the vascular damage contributes substantially to the process of progressive secondary injury culminating in post-traumatic myelopathy. In this study, we found a time-dependent alteration of thromboxane-prostacyclin balance in the injured spinal cord with thromboxane dominance during the first 2 h: a time when maximal vascular injury is reflected by extravasation of 125I-labelled serum albumin. The thromboxane-prostacyclin imbalance reverted to favor prostacyclin by 18 h post-injury. This time-dependent alteration of thromboxane-prostacyclin balance should be considered in the planning of therapeutic attempts to prevent secondary injury by pharmacological modulation of platelet-vessel wall interaction.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Moyamoya disease in Taiwan.

Moyamoya disease occurring in Chinese has been inadequately described. Here we report 13 cases of this disease identified by review of 3,200 cerebral angiograms performed between August 1979 and March 1986. Nine were males and four were females; there were 12 adults (aged 34-51 years) and one child (aged 11 years). All had hemorrhagic strokes with one exception, a patient with an occipital infarction. Intraventricular hemorrhage was noted by computed tomography in 10; five of these emanated from the caudate nucleus. A localized hematoma without intraventricular hemorrhage was found in two. All 13 angiograms had smokelike basal anastomoses with various degrees of stenosis or occlusion of the anterior portion of the circle of Willis; the involvement was bilateral in 12 and unilateral in one. Aneurysms were found in two patients, one in the anterior communicating artery and the other in the left anterior choroidal artery. Eleven patients recovered from the initial stroke, but two died with recurrent hemorrhage. This series differs from the series reported in Japan by the predominance of adult males. The high incidence of intraventricular hemorrhage and intracerebral hematoma is not in keeping with the previous Chinese series, in which subarachnoid hemorrhage was suspected to be the major clinical manifestation.

Adult↗
PubMed1988

Pentoxifylline in acute nonhemorrhagic stroke. A randomized, placebo-controlled double-blind trial.

The efficacy and safety of pentoxifylline were assessed in 297 adult patients with ischemic stroke in a multicenter, double-blind, randomized and placebo-controlled trial. Treatment was started within 12 hours after the stroke onset. Study medication was administered intravenously continuously (16 mg/kg/day, maximum 1,200 mg/day) for 3 days and per os (400 mg t.i.d.) for the remainder of 28 days. Demographic data were comparable, and functional impairment and mortality (pentoxifylline 12%, placebo 10%) were not different between the two groups. Neurologic deficit scores improved from baseline admission scores during the 4-week study in both groups but did not differ between groups at admission or throughout the study except during the first few days when the consciousness level (Days 1 and 2), motor function (Days 1 and 2), cranial nerve function (Days 1-4), and total neurologic deficit scores (Days 1 and 2) were better in the pentoxifylline group than in the placebo group, especially in a subset of patients with severe deficits at admission. Laboratory values and side effects were also comparable between groups. Our study indicates that pentoxifylline can be given safely in patients with acute ischemic stroke. Although pharmacologic effects were present during the first few days, the clinical benefits were small and not sustained.

Acute Disease↗
PubMed1987

In situ visualization of glycosphingolipids on thin-layer chromatograms using lectin-peroxidase conjugates.

A technique is described for direct detection by lectins conjugated to horseradish peroxidase of the oligosaccharides of glycosphingolipids on thin-layer chromatograms. Final visualization is accomplished using a substrate medium consisting of hydrogen peroxide and 3,3'-diaminobenzidine. The procedure is rapid, specific, sensitive and highly reproducible, and staining patterns are stable for years. In addition to providing preliminary structural information, this technique can be employed in combination with other methods, such as autoradiographic detection of tritium-labeled glycosphingolipids in the same chromatogram.

Animals↗
PubMed1987

Distribution of calcium-activated neutral proteinase activity in quaking mouse brain: a subcellular study.

The distribution of calcium-activated neutral proteinase (CANP) activity was examined in the subcellular fractions of quaking and control mouse brain. The CANP activity was determined in purified myelin, cytosol and pellet (P2, consisting of nuclei, mitochondria and microsomes) fractions using [14C]azocasein as substrate. The enzyme activity in quaking brain was 1.3-fold greater than control. Fifty-seven percent of the control brain activity was in purified myelin compared to only 7% in quaking myelin. The specific activity of the control purified myelin was 4-fold greater than homogenate while that of the quaking was two-fold greater. In contrast, 51% of the quaking brain activity was present in cytosol compared to only 18% in the control. Triton X-100 greatly increased the control brain activity (10-fold) while the quaking brain activity was increased by only 1.2-fold. The total calcium content in the quaking brain was greatly elevated (6-fold) compared to control. Approximately 30% of the brain 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) activity was in quaking myelin while 77% of the CNPase activity in control brain was in myelin. These results suggest that in quaking brain much of the CANP is not incorporated into the myelin membrane and remains cytosolic.

2',3'-Cyclic Nucleotide 3'-Phosphodiesterase↗
PubMed1987

Distribution of calcium activated neutral proteinase (mM CANP) in myelin and cytosolic fractions in bovine brain white matter.

The activity of calcium-activated neutral proteinase (mM CANP) was determined in homogenate, myelin and supernatant of bovine brain corpus callosum. The enzyme activity in homogenate and myelin was increased eleven and thirteen-fold respectively by Triton X-100. Myelin prepared by the method of Norton and Poduslo as well as by a modified method, was shown to contain most (more than 50%) of homogenate mM CANP activity. The specific activity was highest in myelin, and increased almost three times more than the homogenate. Supernatant only contained 17% of enzyme activity. It is concluded from these studies that mM CANP is tightly bound to the membrane and predominantly associated with the myelin sheath.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1987

Increased turnover of myelin proteolipid protein in quaking mouse brain.

Homozygous quaking and normal control littermate mice were injected intracerebrally with [3H]leucine at 19 days of age. The animals were sacrificed after 1 h and after 6 days. The proteolipid protein (PLP) and intermediate protein (IP) were extracted from whole brain by chloroform-methanol (2:1) and resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). One hour postinjection the labeling of total protein in quaking brain was the same as the control and the radioactivity of PLP and IP in quaking was approximately 35% of the control. Six days after precursor administration the radioactivity of the total protein decreased significantly in both groups and to the same extent. However, the labeling of PLP and IP more than doubled in the control, while it decreased by half in the quaking brain. The results indicate that there is an increased turnover rate of PLP and IP in quaking brain.

Animals↗
PubMed1987

Ca2+-mediated degradation of central nervous system (CNS) proteins: topographic and species variation.

Incubation of homogenates of rat, rabbit, and bovine spinal cord and of bovine brain white and gray matter in the presence of calcium (5 mM) produced an extensive degradation of the neurofilament triplet proteins (NFP; 200 K, 150 K, and 69 K). The breakdown products of the NFPs were identified by immunoblot. The glial fibrillary acidic protein (GFAP), microtubular proteins (MTP), and myelin proteins were also degraded. The 150 K NFP was more susceptible than the other NFPs. The extent of calcium-mediated degradation was slightly greater with rat spinal cord than the others. Bovine brain white matter had more activity than gray, which had no appreciable degradative activity. The breakdown was prevented by both EGTA and leupeptin but a similar concentration of MgCl2 (5 mM) had no effect. These results suggest that NFPs are degraded by a Ca2+-activated neutral proteinase in the central nervous system (CNS) of several species. The lesser activity in gray matter suggests that the enzyme is enriched in axons, myelin, and/or oligodendroglial cells.

Animals↗
PubMed1987

The multimolecular cascade of spinal cord injury. Studies on prostanoids, calcium, and proteinases.

Experimental spinal cord injury in animals induced by weight drop produces neurological deficit and paralysis. Correlation of the progressive morphological changes in the lesion by both light and electron microscopy with the biochemical alterations revealed ischemia, edema, hemorrhage, tissue necrosis, granular changes in axons, vesicular degeneration of myelin and axonal calcification. The biochemical pathology was that of degradation of axonal (neurofilaments) and myelin proteins (MBP and PLP) with increased activities of proteolytic enzymes and particularly the neutral proteinase. The level of total calcium increased progressively in the lesion to a peak at 8 hrs. and subsequently remained constant thereafter. The capacity of calcium for activating proteinases and lipases and fostering the degradation of axon and myelin proteins as well as the liberation of arachidonic acid required for the synthesis of prostanoids must be relevant. An increased production of prostanoids is indicated by elevation of thromboxane (TxB2), a stable metabolite of TXA2 at 1 hour after injury. The 6-keto-PG1(1)a was also increased but to a lesser extent. We suspect that the activation of arachidonic acid metabolism contributes to post-traumatic vascular injury and the progressive ischemia. These putative roles for calcium in proteolysis and lipolysis, inducing degradation of macromolecules and production of prostanoids which initiate edema, lysolecithin a myelinolytic factor and mitochondrial dysfunction in spinal cord injury are discussed.

Calcium↗
PubMed1987

Therapeutic model for experimental spinal cord injury in the rat: I. Mortality and motor deficit.

In the course of establishing a therapeutic model for experimental spinal cord injury in the rat, we determined the effects of trauma dose (20, 30, 40, 50, and 60 g-cm) on the mortality and motor deficit in the 4 weeks following injury. Mortality was dependent upon the trauma dose: 20 g-cm, 11%; 30 g-cm, 14%; 40 g-cm, 27%; 50 g-cm, 32%; 60 g-cm, 41%. Statistical analysis by linear regression is highly significant for increasing mortality with increasing trauma dose. The motor deficit determined by a modified Tarlov scale also was dependent upon trauma dose. A trauma dose-response curve based on this study indicates that a drug which reduces the motor deficit from that found at 40 g-cm to that at 30 g-cm may be detected at a significant level of 0.05 with a power of 0.8 if 30 rats are included in each of placebo and treated groups. The same sample size would detect a significant reduction of mortality from that of 40 g-cm to 30 g-cm.

Animals↗
PubMed1987

Brain calcium content in ischemic infarction.

Three degrees of focal ischemic infarction in the rat were created in the cerebral cortex supplied by the right middle cerebral artery, by ligation of the right middle cerebral artery and the right common carotid artery and temporary clip compression of the left common carotid artery, in succession. The postischemic accumulation of calcium in cerebral cortex of the right middle cerebral artery territory, determined by atomic absorption spectrometry, correlated with the infarct volume. The results are consistent with the hypothesis that calcium has role as a mediator in the pathogenesis of cerebral infarction.

Animals↗