Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We recently described a monoclonal antibody, 10E5 , that completely blocks adenosine diphosphate (ADP) induced fibrinogen binding to platelets and aggregation induced by ADP, epinephrine, and thrombin. Multiple lines of evidence indicate that 10E5 binds to platelet membrane glycoproteins IIb and/or IIIa. Because it has been reported that platelets treated with chymotrypsin aggregate when fibrinogen is added, we tested the effect of 10E5 antibody on chymotrypsin-induced fibrinogen binding and platelet aggregation. Aspirin-treated human platelets were washed in modified Tyrode's buffer (pH 7.5), incubated for 5 minutes at 22 degrees C with 300 micrograms/mL chymotrypsin, and washed again. The amount of 10E5 antibody bound to these platelets (37,232 +/- 2,928 molecules/platelet; mean +/- SEM, N=9) was similar to that bound to unstimulated control platelets (36,910 +/- 2,669) and did not differ significantly from the amount of antibody bound to ADP-treated platelets (P less than .01, N = 5). The amount of 10E5 bound to chymotrypsin-treated platelets correlated directly with the amount of fibrinogen bound to separate aliquots of the same platelet samples (r = .876, P less than .001). The 10E5 antibody caused virtually complete inhibition of both the binding of fibrinogen to chymotrypsin-treated platelets and the aggregation induced by exogenous fibrinogen. Immunoprecipitation studies of 125I-labeled chymotrypsin-treated platelets revealed that the 10E5 antibody bound proteins with molecular weights characteristic of glycoproteins IIb and IIIa. These data suggest that the fibrinogen receptor on chymotrypsin-treated platelets is identical to that on ADP-treated platelets and that this receptor is either near to, or on, the glycoprotein IIb/IIIa complex.
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PMID:A murine monoclonal antibody that blocks fibrinogen binding to normal platelets also inhibits fibrinogen interactions with chymotrypsin-treated platelets. 673 83

Fibronectin has been localized to basement membranes and cell surfaces with the light microscope by fluorescent staining of thick sections, and with the TEM by immunoperoxidase reaction. However, these methods are limited because it is difficult to appreciate the patterned distribution of fibronectin from sectioned material. We have developed a probe for fibronectin that facilitates its identification with the SEM. Our probe consists of two parts; the first component is a derivatized methacrylate microsphere 90 nm in diameter, linked to purified sheep anti-rabbit IgG. The second component is anti-fibronectin IgG raised in rabbits. Stage-3 to -12 chick embryos were fixed and the ectoderm covering the cranial mesoderm was removed. Embryos were treated with testicular hyaluronidase, exposed to rabbit anti-fibronectin IgG and finally to sheep anti-rabbit IgG conjugated microspheres. As expected, the basal lamina of surface and neural ectoderm as well as the remaining fibrous ECM were heavily decorated with microspheres, whereas control embryos treated with preimmune serum were beadless. Fibronectin was localized on the cell soma and processes of primary mesenchyme as early as stage 3. In addition, it was possible to decorate to various extents, populations of prosencephalic, mesencephalic, and rhombencephalic cranial neural crest cells. Our studies suggest that fibronectin is present in the cranium of chick embryos at earlier times than heretofore realized, and that fibronectin accumulates in a cranial to caudal gradient that reflects the sequential differentiation of the embryonic axis.
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PMID:SEM localization of cell-surface-associated fibronectin in the cranium of chick embryos utilizing immunolatex microspheres. 674 25

The neuromuscular sensitivity of 71 patients (A.S.A. class I or II) was tested by scoring on a scale from 1 to 6 the ability to lift the upper eyelid 2 minutes after pretreatment with 1 mg of pancuronium. Subsequently, each patient also received an additional "intubation dose" pancuronium (in milligrams) equal to the eye-opening test score (group I), or either 1 mg (group II) or 2 mg (group III) in excess. The resultant depression of the neurally evoked muscle response of the little finger was quantified by another score (the response score) which allowed for assessment of neuromuscular block beyond the limit of 100% depression of the twitch. The criteria for the response score, in the response score, in the order of increasing magnitude of block, were: (1) visible twitch responses to all 4 of the train-of-four stimulation remained; (2) part of the train-of-four twitches was eliminated; (3) all twitches were eliminated; (4) tetanus was eliminated; (5) post-tetanic twitch following a 5-second 50 Hz tetanus was also eliminated; and (6) not even the post-tetanic twitch became elicitable again in 30 minutes. It was found that 1 mg of pancuronium depressed the eye-opening score to 4.0 +/- 0.2, from 5.1 +/- 0.1 (mean +/- SEM, p < 0.01). Following the additional "intubation dose" of pancuronium, patients in group I had an average response score of 2.2 +/- 0.3, those in group II a score of 3.4 +/- 0.2, and those in group III, a score of 4.8 +/- 0.6. Each additional 1 mg of pancuronium (increasing from group I to III) linearly increased the average response score. In terms of frequency response, patients in group I had more than a 50% change of being scored 1, while those in group II had a greater than 50% chance of being scored 3, 4, or 5, and those in group III had more than a 50% chance of being scored 6. It is concluded that sensitivity to pancuronium can be quantified by the ptotic response to a 1-mg test dose of pancuronium, and that a sensitivity-adjusted additional "intubation dose" of pancuronium can be predetermined in individual patients.
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PMID:Predetermination of dose requirement of pancuronium. 719 44

Rabbit anti-human platelet antiserum (RPA) has been shown to mediate human platelet aggregation and 14C-serotonin release. This effect is not inhibited by aspirin. However, it is not known whether antibody induces platelet prostaglandin synthesis. We, therefore, investigated the effect of RPA on human platelets by measuring malondialdehyde (MDA) production as a reflection of prostaglandin synthesis and comparing it with 14C-serotonin release. Independently, ATP release was also measured as a further measure of platelet secretion. Normal rabbit serum did produce a small amount of MDA (0.54 +/- 0.09 SEM nmole/10(9) platelets). However, RPA produced a much larger amount of MDA (1.43 +/- 0.18 nmole/10(9) platelets) and pre-incubation with aspirin significantly decreased MDA production (0.16 +/- 0.07 nmole/10(9) platelets) (p less than .001). Aspirin did not significantly impair the capacity of RPA to release 14C-serotonin or ATP. These results demonstrate that prostaglandin synthesis occurs when heterologous antibody is added to human platelets. However, prostaglandin formation must be a secondary event in this process since the inhibition of prostaglandin synthesis by aspirin had little effect on the ability of RPA to induce 14C-serotonin release or ATP release.
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PMID:Effect of heterologous antibody on human platelet prostaglandin synthesis. 736 55

Reaction times for schizophrenic individuals in a simple visual tracking experiment can be substantially more variable than for non-schizophrenic individuals. Current psychological theory suggests that at least some of this extra variability arises from an attentional lapse that delays some, but not all, of each schizophrenic's reaction times. Based on this theory, we pursue models in which measurements from non-schizophrenics arise from a normal linear model with a separate mean for each individual, whereas measurements from schizophrenics arise from a mixture of (i) a component analogous to the distribution of response times for non-schizophrenics and (ii) a mean-shifted component. We fit four mixture models within this framework, where the distinctions between models arise from assumptions about the variance of the shifted observations and the exchangeability of schizophrenic individuals. Some of these models can be fit by maximum likelihood using the EM algorithm, and all can be fit using the ECM algorithm, where the covariance matrices associated with the parameters are calculated by the SEM and SECM algorithms, respectively. Bayesian model monitoring using posterior predictive checks is invoked to discard models that fail to reproduce certain observed features of the data and to stimulate the development of better models.
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PMID:The analysis of repeated-measures data on schizophrenic reaction times using mixture models. 764 56

We tested whether a high spinal anesthesia may alter the susceptibility to the soporific effects of sedatives. Twenty ASA grade I and II women undergoing elective abdominal hysterectomy were randomly allocated into two groups. Patients in Group I were given a subarachnoid injection of 12 mg hyperbaric tetracaine and those patients who after 10 min had a sensory level of T4-6 (10 patients) were included in the study. Ten additional patients (Group II) received no spinal injection. Induction of anesthesia was performed on all patients by injecting 1 mg of midazolam intravenously every 30 s until the patient failed to respond to three repeated commands to squeeze the anesthetist's hand. This was considered the induction dose or end-point for the purposes of the study. Patients were then given a neuromuscular blocker, ventilated with oxygen, nitrous oxide, and a volatile anesthetic, tracheally intubated, and maintained under general anesthesia for the remainder of the operation. The dose of midazolam administered to the point of patient failure to respond to command was 7.6 +/- 0.72 mg SEM for Group I and 14.7 +/- 1.16 mg SEM for Group II, (P < 0.0001). These results support the conclusion that patients having a high spinal anesthetic are more sensitive to the sedative effects of midazolam.
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PMID:The influence of high spinal anesthesia on sensitivity to midazolam sedation. 865 49

Early stage embryos of the starfish Pisaster ochraceus exhibit one cilium per cell which is primarily involved in locomotion. SEM observations have demonstrated two types of microvilli "stage horn"-like and "finger-like" microvilli (CMs), both of which probably serve to anchor and support the hyaline layer (HL). The CMs arise from the cellular membrane a short distance from the base of the ciliary shaft and form a circle around the base of each cilium. This arrangement is found in embryos and larvae as well as in adult tissues of many other marine organisms. TEM observations of material prepared by freeze substitution has demonstrated that the HL unites the circle of CMs and forms two collars. The outer ECM collar is single and attached directly to the CMs, while the inner collar consists of multiple rings of ECM located between the cilium and the CMs. The inner collar elements are not attached to the cilium but are attached to the inner aspects of the CMs by a complex arrangement consisting of a loop of ECM and two short ECM fibers. The arrangement of the ECM of the collars could provide an excellent way to transmit the movements of the cilium to the surrounding microvilli. Although the bases of the CMs always encircle the ciliary shaft, the shafts of the CMs are seen in different positions. This suggests that the CM/ECM collar may be able to change position relative to the cilium. Confocal laser scanning microscopy demonstrates that the CMs contain phalloidin positive material which extends into a phalloidin positive region located in the apex of the cells. The CMs and apical web contain microfilaments which are probably actin and could be involved in movement of the CMs. A movable circle of CMs with their associated ECM could represent a mechanism to sense the position of the cilium and/or to define the direction and extent of the stroke.
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PMID:The microvilli and hyaline layer of embryonic asteroid epithelial collar cells: a sensory structure to determine the position of locomotory cilia? 769 Oct 38

Blood cell aggregates are thought to be the cause of spontaneous echo contrast (SEC), although there is disagreement as to whether red cell or platelet aggregates produce this effect. One way to differentiate between these 2 possibilities is to evaluate the effect of aspirin on SEC because aspirin would not be expected to affect red cell aggregates. To eliminate the need to perform repetitive transesophageal echocardiographic studies, and the possible effect of the underlying disease process on SEC, the effect of aspirin on SEC in the brachial vein was studied in normal volunteers using a single-blind, before-and-after study design. Other factors known to affect blood echogenicity including hematocrit, sedimentation rate, and the presence of platelet aggregates by microscopy were also studied. The amount of SEC was quantitated by image analysis and expressed as the aggregate score. The results in 10 volunteers showed that all had SEC in brachial veins before aspirin, but there was no significant day-to-day variation in the amount of SEC during the control period (mean +/- SEM 104,248 +/- 23,088, 153,722 +/- 35,664, and 124,568 +/- 22,827 for days 1, 3, and 5, respectively). A significant decrease in the aggregate score occurred after 7 days of aspirin, 650 mg twice a day (51,690 vs 127,513, p = 0.002); this was accompanied by a striking decrement in the size of the largest platelet aggregate found in venous blood. Aspirin caused no significant change in the hematocrit or sedimentation rate. These results indicate that there is a component of SEC that is aspirin-sensitive and is likely to represent platelet aggregates.
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PMID:Effect of aspirin on spontaneous contrast in the brachial veins of normal subjects. 773 2

Sevoflurane, a new volatile inhalational agent, undergoes biotransformation to fluoride which is potentially nephrotoxic. We compared the effects of sevoflurane or isoflurane anaesthesia on hepatorenal function and serum fluoride concentrations in 50 ASA 1-3 patients undergoing major intra-abdominal surgery. No patient developed renal or hepatic dysfunction. Mean (SEM) peak fluoride concentrations were 23.1 (1.5) mumol.l-1 for sevoflurane and 5.4 (0.4) mumol.l-1 for isoflurane (p < 0.001). There was a significant correlation in the sevoflurane group between the total dose of agent (MAC h), the total fluoride production (r = 0.78, p = 0.0001) and peak fluoride concentration (r = 0.57, p = 0.003). There was no correlation between these variables in the isoflurane group.
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PMID:Circulating fluoride changes and hepatorenal function following sevoflurane anaesthesia. 780 35

Recovery after doxacurium and pancuronium neuromuscular blockade and their acceleration by neostigmine have not been compared in children. Therefore, 60 paediatric surgical patients aged 2-10 yr (ASA 1-2) were studied. They were randomized to receive doxacurium 30 micrograms.kg-1 or pancuronium 70 micrograms.kg-1 iv during propofol, fentanyl, isoflurane and nitrous oxide anaesthesia. Electromyographic (EMG) responses of the adductor pollicis to train-of-four (TOF) stimulation of the ulnar nerve were recorded every ten seconds using a Datex NMT monitor. Six patients in each relaxant group received neostigmine (0, 5, 10, 20 or 40 micrograms.kg-1) with atropine by random allocation when first twitch height (T1) had recovered to 25% of control. Spontaneous recovery after ten minutes was similar following doxacurium (mean +/- SEM values of 45.0 +/- 3.9 vs 49.5 +/- 10.0% for T1 and 25.2 +/- 3.8 vs 14.8 +/- 3.6% for TOF ratios). Dose-responses to neostigmine were calculated from the log dose vs logit of T1 or TOF ratio after ten minutes. Neostigmine-assisted recovery was not different in the two groups, with ED70 and ED90 doses for T1 of 14.3 +/- 1.8 and 25.7 +/- 2.7 micrograms.kg-1 for doxacurium and 12.5 +/- 1.7 and 25.3 +/- 2.3 micrograms.kg-1 for pancuronium. Time to recovery of TOF ratio to 70% after neostigmine 40 micrograms.kg-1 was 2.3 +/- 1.0 and 4.2 +/- 1.7 min (P = NS) following pancuronium and doxacurium, respectively. Adjusted recovery due to neostigmine alone (spontaneous recovery subtracted from the total) required two to three times higher doses of neostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversal of doxacurium and pancuronium neuromuscular blockade with neostigmine in children. 782 55


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