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C Werner

Publications and source records attributed to C Werner.

At least 19 recordsLinked to original sources
PubMed1992

Comparison of the body wall myosin heavy chain sequences from Onchocerca volvulus and Brugia malayi.

The complete coding sequence of Onchocerca volvulus myosin heavy chain has been determined from a series of overlapping cDNAs. The protein sequences from the 2 filarids, one responsible for subcutaneous filariasis, the other for lymphatic filariasis, show 92% identity, and are 1957 amino acids long. Each protein sequence is also equally related, with 75% identity, to MHC-B, the protein encoded by the unc-54 gene of the free-living nematode C.elegans. Such analysis is useful in phylogenetic studies among nematodes, as well as in structure-function relationships among myosin isolates.

Amino Acid Sequence↗
PubMed1992

Characterization of a myosin heavy chain gene from Brugia malayi.

We have previously shown that an antigen recognized by antibodies in sera of several microfilaremic individuals from a Wuchereria bancrofti endemic area bears strong homology to an invertebrate muscle protein. We have cloned and sequenced the entire gene containing this antigen encoding fragment and present data that confirms that the antigen is myosin heavy chain (MHC). This gene, which we have named Bmmyo-1 extends over 11 kb and has the potential to encode a protein of 1957 amino acids. The coding sequence is interrupted by 14 introns, most of which are larger than those in the myosin gene of the free-living nematode, Caenorhabditis elegans. The protein encoded by this gene bears greatest homology (75.1% identity) to the C. elegans myosin isoform MHC-B, encoded by the unc-54 gene. MHC-B is the major body wall myosin in C. elegans.

Amino Acid Sequence↗
PubMed1992

The effects of propofol on brain electrical activity, neurologic outcome, and neuronal damage following incomplete ischemia in rats.

This study compares the effects of propofol and fentanyl/N2O on spontaneous brain electrical activity, neurologic outcome, and neuronal damage due to incomplete cerebral ischemia in rats. Thirty Sprague-Dawley rats were assigned to one of three groups: group 1 (n = 10) received 70% N2O in O2 plus fentanyl (bolus 10 micrograms.kg-1, infusion 25 micrograms.kg-1.h-1); group 2 (n = 10) received 70% N2 in O2 and propofol (infusion 0.8-1.2 mg.kg-1.min-1) adjusted to maintain EEG burst suppression during ischemia; group 3 (n = 10) was anesthetized with propofol and received 6 ml.kg-1 10% glucose intraperitoneally 15 min before the start of ischemia. Incomplete cerebral ischemia was produced by right common carotid artery occlusion combined with hemorrhagic hypotension (35 mmHg) for 30 min. Arterial blood gases, pH, and rectal temperature were kept constant in all groups. Plasma glucose was lower during ischemia in propofol-anesthetized rats compared to that in fentanyl/N2O- (P = 0.009) and glucose-loaded propofol-treated rats (P = 0.008). Neurologic outcome and brain tissue injury were significantly better in propofol-anesthetized compared to fentanyl/N2O-anesthetized rats (P less than 0.05). Elevated plasma glucose in propofol-treated rats resulted in similar neurologic outcome and histopathologic injury as seen in propofol-anesthetized rats given no glucose. Recovery of EEG theta-alpha activity after ischemia was inversely correlated to neurologic deficit (fentanyl/N2O: r = -0.71; propofol: r = -0.83; P less than 0.01). These results show that propofol improves neurologic outcome and decreases neuronal damage from incomplete cerebral ischemia when compared to fentanyl/N2O. This effect is not dependent on plasma glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Ketamine decreases plasma catecholamines and improves outcome from incomplete cerebral ischemia in rats.

Central neuroexcitatory receptors (N-methyl-D-aspartate [NMDA], non-NMDA) may affect outcome from cerebral ischemia by altering sympathetic nervous system activity. We tested whether ketamine, an NMDA antagonist, and NBQX, a non-NMDA antagonist, improve outcome from incomplete cerebral ischemia in the rat and whether a change in outcome is related to changes in plasma catecholamines. There were five treatment groups: group 1 (control, n = 10) received a fentanyl infusion at a rate of 25 microgram.kg-1.h-1 and ventilation with 70% N2O in O2. Group 2 (n = 10) received the same anesthetic treatment and were given an intraperitoneal injection of 30 mg/kg NBQX 15 min prior to ischemia. Group 3 (n = 10) received a ketamine infusion of 1.0 mg.kg-1.min-1 and ventilation with room air. Group 4 (n = 10) received a ketamine infusion of 1.5 mg.kg-1.min-1. Group 5 received a ketamine infusion of 1 mg.kg-1.min-1 plus a 6 ml/kg intraperitoneal injection of 40% glucose solution 15 min before the start of ischemia. Ischemia was produced by right common carotid ligation combined with hemorrhagic hypotension to 35 mmHg for 30 min. Blood gases, pH, and skull temperature were controlled during ischemia. Plasma glucose increased during ischemia in all groups but was lower in ketamine-anesthetized rats (groups 3 and 4). Glucose-loaded ketamine-anesthetized rats (group 5) had plasma glucose concentrations similar to the control group. Plasma epinephrine and norepinephrine concentrations were significantly less in ketamine-anesthetized rats (groups 3, 4, and 5) during ischemia compared to controls (P less than 0.05). Neurologic outcome was significantly better (P less than 0.05) in all ketamine-treated rats (groups 3, 4, and 5) compared to the control group, regardless of plasma glucose concentration during ischemia. NBQX did not improve neurologic outcome. These results suggest that ketamine improves neurologic outcome from incomplete cerebral ischemia by a mechanism related to a decrease in plasma catecholamine activity.

Animals↗
PubMed1992

[The effect of sufentanil on regional and global cerebral circulation and cerebral oxygen consumption in the dog].

The intracranial hemodynamic and metabolic effects of 20 micrograms/kg sufentanil were studied in ten mongrel dogs. Anesthesia was maintained with 0.7 vol.% end-tidal isoflurane and 50% nitrous oxide in oxygen. Catheters were inserted into both femoral arteries and veins, the superior sagittal sinus, the left atrium, and the lateral cerebral ventricle for blood pressure measurement, arterial and sagittal sinus blood sampling, radioactive microsphere injections, and intracranial pressure (ICP) monitoring. Cardiac output (CO) was measured using an electromagnetic flow probe on the pulmonary artery. Following baseline measurements, sufentanil was injected and data were recorded at 5, 15, and 30 min. RESULTS. In group 1 (n = 5) blood pressure was not controlled, while in group 2 (n = 5) blood pressure was maintained at baseline level with a phenylephrine infusion. Arterial blood pressure decreased by 32% in response to sufentanil in group 1 and remained constant in group 2 according to the protocol. CO decreased by 40%-50% in both groups. Regional and global cerebral blood flow (CBF) decreased by 25%-40% with no difference between groups. The cerebral hemodynamic changes were associated with a decrease of 35%-40% in cerebral oxygen consumption. ICP did not change over time. DISCUSSION. These data are in contrast to studies in dogs, where sufentanil produced non-dose-dependent increases in CBF and ICP. Our results are more consistent with studies in humans and rats where administration of sufentanil was associated with either no change or decreases in cerebral hemodynamics, metabolism, and ICP. We conclude that in dogs with normal intracranial physiology sufentanil decreases regional and global CBF in response to a decrease in cerebral metabolic demand without significantly affecting ICP.

Analgesics, Opioid↗
PubMed1991

Mapping sequenced E.coli genes by computer: software, strategies and examples.

Methods are presented for organizing and integrating DNA sequence data, restriction maps, and genetic maps for the same organism but from a variety of sources (databases, publications, personal communications). Proper software tools are essential for successful organization of such diverse data into an ordered, cohesive body of information, and a suite of novel software to support this endeavor is described. Though these tools automate much of the task, a variety of strategies is needed to cope with recalcitrant cases. We describe such strategies and illustrate their application with numerous examples. These strategies have allowed us to order, analyze, and display over one megabase of E. coli DNA sequence information. The integration task often exposes inconsistencies in the available data, perhaps caused by strain polymorphisms or human oversight, necessitating the application of sound biological judgment. The examples illustrate both the level of expertise required of the database curator and the knowledge gained as apparent inconsistencies are resolved. The software and mapping methods are applicable to the study of any genome for which a high resolution restriction map is available. They were developed to support a weakly coordinated sequencing effort involving many laboratories, but would also be useful for highly orchestrated sequencing projects.

Base Sequence↗
PubMed1991

Concurrent increases in brain electrical activity and intracranial blood flow velocity during low-dose ketamine anaesthesia.

The purpose of the present study was to assess the effects of low-dose ketamine on spontaneous brain electrical activity (EEG) and intracranial blood flow velocity. Twenty healthy volunteers were divided into two groups: Group I (n = 10) received 0.25 mg.kg-1 ketamine iv; Group II (n = 10) received 0.5 mg.kg-1 ketamine iv. Mean arterial blood pressure (MAP), heart rate (HR), end-tidal PCO2 (PETCO2), and arterial oxygen saturation (SaO2) were measured. The EEG was recorded from temporo-occipital recording sites over both hemispheres. Blood flow velocity in the middle cerebral artery was measured using a transcranial Doppler ultrasound system. All variables were evaluated at baseline and for 60 min following ketamine. Administration of ketamine resulted in increases of MAP and HR in both groups to a similar degree. The PETCO2 and SaO2 did not change in either group over time. Ketamine caused a dose-dependent, transient shift in the EEG to synchronous high-voltage slow waves with an increase in total power (Group I: 301 +/- 38%; Group II: 104 +/- 28%). These changes were associated with dose-dependent increases in mean blood flow velocity (Group I: 35 +/- 7%; Group II: 68 +/- 10%). Our data suggest that increases in intracranial blood flow velocity are closely correlated to increases in neuronal activity and are not secondary to changes in systemic haemodynamic variables.

Adult↗
PubMed1991

Isolation and partial sequence of a collagen gene from the human filarial parasite Brugia malayi.

We report the isolation and sequence of a part of a gene encoding a collagen from the genome of the human filarial parasite Brugia malayi. The deduced amino acid sequence of the sequenced portion of this gene, which we have designated BmCol1, differs from the most catalogued nematode collagens in that it is composed predominantly of the glycine-X-Y motif, where either X or Y (or both) may be proline. The gene appears to be similar to two recently described Caenorhabditis elegans collagen genes whose deduced amino acid sequences resemble mammalian basement membrane collagens. BmCol1 is a single copy gene and appears to be present in several other parasitic nematodes examined.

Amino Acid Sequence↗
PubMed1991

Dexmedetomidine improves neurologic outcome from incomplete ischemia in the rat. Reversal by the alpha 2-adrenergic antagonist atipamezole.

Dexmedetomidine is an alpha 2-adrenergic agonist that decreases central sympathetic activity and reduces the anesthetic requirement for halothane. We evaluated the effect of dexmedetomidine on neurologic and histopathologic outcome from incomplete cerebral ischemia in the rat. Anesthesia was maintained with a 25-micrograms.kg-1.h-1 fentanyl infusion combined with 70% nitrous oxide. Incomplete ischemia was produced by unilateral carotid artery ligation combined with hemorrhagic hypotension to 35 mmHg for 30 min. Arterial blood gas tensions, pH, and head temperature were maintained at normal levels during the experiment. Four ischemic groups were tested: group 1 (n = 15) received an intraperitoneal (ip) saline injection (control); group 2 (n = 10) received an ip injection of 10 micrograms/kg dexmedetomidine 30 min before ischemia; group 3 (n = 10) received 100 micrograms/kg dexmedetomidine; and group 4 (n = 10) received 100 micrograms/kg dexmedetomidine plus 1 mg/kg atipamezole (an alpha 2-adrenergic antagonist). Neurologic outcome was evaluated for 3 days using a graded deficit score. Histopathology was evaluated in coronal section in caudate and hippocampal tissue segments. Dexmedetomidine (10 and 100 micrograms/kg) significantly decreased plasma catecholamines and improved neurologic and histopathologic outcome in a dose-dependent manner compared to control rats (P less than 0.05). Atipamezole abolished the decrease in catecholamines and the improvement in outcome seen with dexmedetomidine, confirming that these effects were mediated by alpha 2-adrenergic receptors. It is concluded that alpha 2-adrenoreceptor stimulation decreases sympathetic activity and decreases ischemic injury in a model of incomplete cerebral ischemia.

Adrenergic alpha-Agonists↗
PubMed1991

Captopril improves neurologic outcome from incomplete cerebral ischemia in rats.

We investigated the effects of the angiotensin-converting enzyme inhibitor captopril on neurologic outcome in a rat model of incomplete cerebral ischemia. Twenty male Sprague-Dawley rats were anesthetized with 70% nitrous oxide in oxygen and fentanyl (10 micrograms x kg-1 i.v. bolus, 25 micrograms x kg-1 x hr-1 i.v. continuous infusion). Animals in group 1 (n = 10) received no angiotensin-converting enzyme inhibitor while animals in group 2 (n = 10) were given 10 mg x kg-1 i.v. captopril 30 minutes prior to the ischemic period. Ischemia was produced by unilateral carotid artery ligation and hemorrhagic hypotension to 35 mm Hg for 30 minutes. Body temperature, arterial blood gases, and arterial pH were maintained constant. Neurologic outcome was evaluated every 24 hours for 3 days using a graded deficit score (0, normal; 18, stroke-related death). On the third day after ischemia, captopril significantly improved neurologic outcome (median deficit score = 4) compared with controls (median deficit score = 18) (p less than 0.05). These results suggest that reduced angiotensin II levels or increased tissue kinin concentrations may decrease ischemic brain injury.

Animals↗
PubMed1991

Effects of sufentanil on cerebral blood flow, cerebral blood flow velocity, and metabolism in dogs.

The intracranial and systemic hemodynamic effects of sufentanil (20 micrograms/kg) were studied in 10 mongrel dogs. Baseline anesthesia was maintained with 0.7% end-tidal isoflurane and 50% nitrous oxide in oxygen. Catheters were inserted for blood pressure measurement, arterial and sagittal sinus blood sampling, radioactive microsphere injections, and intracranial pressure monitoring. Blood flow velocity was measured continuously in the middle cerebral artery using a transtemporal approach through a cranial window with a pulsed 8 MHz transcranial Doppler system (TCD). Cardiac output was measured using an electromagnetic flow probe on the pulmonary artery. After baseline measurements, sufentanil was injected and data were recorded at 5, 15, and 30 min. In group 1 (n = 5) blood pressure was not controlled, whereas in group 2 (n = 5) blood pressure was maintained at baseline levels with a phenylephrine infusion. Sufentanil decreased blood pressure from 120 +/- 10 mm Hg (mean +/- SEM) to 82 +/- 11 mm Hg in group 1. Cardiac output decreased 40%-50% in both groups. Intracranial pressure did not change. Cerebral blood flow (CBF) and TCD blood flow velocity decreased significantly (35%-40%) with no difference between groups. Relative decreases in CBF and TCD blood flow velocity were closely correlated (r = 0.82). The cerebral hemodynamic changes were associated with a 35%-40% decrease in cerebral oxygen consumption. We conclude that sufentanil decreases CBF in response to decreased metabolic demand without significantly affecting intracranial pressure. Relative changes in CBF can be reproducibly monitored using TCD.

Anesthesia, Inhalation↗
PubMed1991

Cerebral autoregulation in awake versus isoflurane-anesthetized rats.

We evaluated regional cerebral and spinal cord blood flow in rats during isoflurane anesthesia. Tissue blood flow was measured in cerebral cortex, subcortex, midbrain, and spinal cord using radioactive microspheres. Blood flow autoregulation was measured within the following arterial blood pressure ranges (mm Hg): 1 = less than 50, 2 = 50-90, 3 = 90-130, 4 = 130-170, 5 = greater than 170. Arterial blood pressure was increased using phenylephrine infusion and decreased with ganglionic blockade and hemorrhage. Three treatment groups were studied: 1 = awake control, 2 = 1.0 minimum alveolar anesthetic concentration (MAC) isoflurane, 3 = 2.0 MAC isoflurane. Autoregulation was seen in awake rats from 50 to 170 mm Hg in all tissues. The autoregulatory coefficient (change in blood flow/change in blood pressure) was increased in midbrain and spinal cord during 1.0 MAC isoflurane and in all tissues during 2.0 MAC isoflurane (P less than 0.05). Within the arterial blood pressure range of 90-130 mm Hg, isoflurane produced the following changes in tissue blood flow (percent of awake control): 1.0 MAC isoflurane: cortex = 87% +/- 8% (P greater than 0.30), subcortex = 124% +/- 11% (P greater than 0.05), midbrain = 263% +/- 20% (P less than 0.001), spinal cord = 278% +/- 19% (P less than 0.001); 2.0 MAC isoflurane: cortex = 137% +/- 13% (P less than 0.05), subcortex = 272% +/- 24% (P less than 0.001), midbrain = 510% +/- 53% (P less than 0.001), spinal cord = 535% +/- 50% (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1990

Hepatic uptake and antihepatotoxic properties of vitamin E and liposomes in the mouse.

Intravenous administration of soybean phosphatidylcholine liposomes containing different amounts of tocopherol acetate leads to a dose and time dependent increase of mouse liver tocopherol content, which was not observed when the preparation was given orally. When benzo[a]pyrene pretreated mice intoxicated with 400 mg/kg AAP were pretreated 2 h before with 1 g/kg phosphatidylcholine liposomes containing 4 mg/kg vitamin E acetate, these animals were protected against liver damage. Vitamin E alone or liposomes lacking vitamin E showed no protection. In an inflammatory liver disease model, i.e. fulminant hepatitis induced by intraperitoneal administration of 700 mg/kg galactosamine and 1 microgram/kg lipopolysaccharide phosphatidylcholine liposomes protected at a dose of 1 g/kg i.v. In this case, however, the protection was not due to the presence of vitamin E. These findings demonstrate the usefulness of phosphatidylcholine for liver protection and show that the protective spectrum is improved when they contain vitamin E. The data suggest that phosphatidylcholine is an excellent carrier for delivery of vitamin E to the liver.

Acetaminophen↗
PubMed1990

Isolation and characterization of a repetitive DNA element from the genome of the human filarial parasite, Brugia malayi.

The genome of the human filarial parasite Brugia malayi contains at least two major repetitive DNA elements. One, referred to as the HhaI family, consists of 10(4)-10(5) tandemly arrayed copies per haploid genome of a monomer of 322 base pairs and does not contain a cleavage site for the restriction endonuclease MboI. We constructed a library of MboI-digested genomic B. malayi DNA in BamHI-cut M13mp18 resulting in the exclusion of the HhaI repeat family from the library. Hybridization of this genomic library with nick-translated genomic DNA yielded several copies of a repeat family which we have named the BmMboI family. From sequence analysis of more than 50 monomers, which differ from each other in sequence and length, we have been able to divide the monomers into several regions based on the level of sequence conservation. Southern blot analyses of B. malayi genomic DNA digested with a variety of restriction endonucleases and probed with the isolated repeat demonstrate multiple bands of varying sizes except with HindIII-cut DNA, where the repeat is found only in very high-molecular-weight DNA.

Animals↗
PubMed1990

[Changes in blood flow velocity in the basal cerebral arteries following neck dissection].

Cerebral blood-flow velocities (cm/s) and pulse index (PI) were studied pre- and postoperatively in a total of 15 male patients following bilateral radical/functional (group A; n = 10) or unilateral radical neck dissection (group B; n = 5) using a 2 MHz-pulsed transcranial Doppler ultrasonographical system (TCD), with a transtemporal approach to the middle cerebral artery. Systolic and mean flow velocities were significant reduced with subsequent increases in PI during the first postoperative sonography in group A-patients while no significant differences in TCD date developed in group B. Blood-flow velocities and PI reached control values within three days. General hemodynamic and respiratory parameters did not influence the changes in TCD flow profiles with the exception of moderate increases in arterial CO2 during the early postoperative period. It is concluded that the reductions in blood-flow velocities and concomitant increases in PI reflect a heightened resistance to flow in the arterial cerebral vasculature. The decrease in cerebral vascular compliance suggests increases in the cerebral venous outflow following the resection of essential drainage pathways. However, TCD does not provide any information about the adequacy of cerebral blood flow.

Adult↗
PubMed1990

Ganglionic blockade improves neurologic outcome from incomplete ischemia in rats: partial reversal by exogenous catecholamines.

The authors investigated the effects of nitrous oxide (N2O), ganglionic blockade, and combined infusion of epinephrine and norepinephrine (0.1 microgram.kg-1.min-1 each) on neurologic outcome and brain histopathology in a model of incomplete cerebral ischemia in the rat. Thirty-eight Sprague-Dawley rats were assigned to one of four groups: group 1 (n = 10) received 70% N2O in O2; group 2 (n = 12) received 70% N2O in O2, plus ganglionic blockade; and group 3 (n = 10) received 70% N2O in O2, plus ganglionic blockade and catecholamine infusion. In groups 1-3, ischemia was produced by right carotid occlusion combined with hemorrhagic hypotension (35 mmHg) for 30 min. Group 4 (n = 6) received 70% N2O in O2 and hemorrhagic hypotension without carotid occlusion for 30 min. At the end of ischemic and nonischemic hypotension, the carotid artery was unclamped and the blood slowly reinfused. Neurologic outcome was evaluated for a 5-day period with a graded deficit score (0 = normal to 39 = stroke-related death). Brain histopathology was evaluated in coronal section at the level of the caudate nucleus according to a 6-point scale, from 0 = normal to 5 = total hemispheric infarction. Arterial blood gases, pH, and body temperature were kept constant in all groups. Compared to N2O alone (group 1), treatment with ganglionic blockade (group 2) decreased plasma catecholamines by 75% and significantly improved neurologic outcome from incomplete cerebral ischemia (P less than 0.05). Administration of exogenous epinephrine and norepinephrine in the presence of N2O and ganglionic blockade (group 3) worsened neurologic outcome compared to group 2 (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Impact of magnesium supplementation on performance data in young swimmers.

We examined whether healthy young swimmers improved performance during emotional and physical stress testing in the laboratory or during competition. Twenty four well trained healthy Caucasian pupils (14 boys and 10 girls, means = 16 years) were randomly treated either with 20 mmol Mg-aspartate-HCl/d or placebo for 3 months. After Mg supplementation serum Mg increased from 0.85 +/- 0.03 to 0.89 +/- 0.06 mmol/litre (P less than 0.05). Mg in red blood cells remained unchanged (4.79 +/- 0.35 mmol/kg dry weight before supplementation and 4.96 +/- 0.27 three months later, P = 0.32) whereas no increase in serum Mg or Mg in red blood cells was found in subjects who received placebo. Student's t test and analyses of variance revealed no significant differences in performance data either in the laboratory or during competition after supplementation with Mg.

Adolescent↗