Magic words.
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Emergency Medical Technicians↗
Biomedical subjects
M Smith
Publications and source records attributed to M Smith.
Production of hydroxy fatty acids in the seeds of Arabidopsis thaliana.
Seed-specific expression in Arabidopsis thaliana of oleate hydroxylase enzymes from castor bean and Lesquerella fendleri resulted in the accumulation of hydroxy fatty acids in the seed oil. By using various Arabidopsis mutant lines it was shown that the endoplasmic reticulum (ER) n-3 desaturase (FAD3) and the FAE1 condensing enzyme are involved in the synthesis of polyunsaturated and very-long-chain hydroxy fatty acids, respectively. In Arabidopsis plants with an active ER Delta12-oleate desaturase the presence of hydroxy fatty acids corresponded to an increase in the levels of 18:1 and a decrease in 18:2 levels. Expression in yeast indicates that the castor hydroxylase also has a low level of desaturase activity.
Arabidopsis↗
It's all about speed. Interview by Fred D. Baldwin.
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Decision Support Systems, Clinical↗
Clinical trials referral resource. Current clinical trials in pediatric acute lymphoblastic leukemia.
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Adolescent↗
In the trenches of private practice. One NP's struggle.
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Humans↗
Alcohol misuse--perspectives from the other side.
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Alcoholism↗
Anticholinesterases in the treatment of Alzheimer's dementia--the first year's experience in Argyll & Clyde.
The local experience of the introduction of a new anticholinesterase treatment for Alzheimer's dementia is described, including the use of a protocol to introduce the use of these drugs. The results in the first 233 patients seen are reported. The protocol seemed to anticipate SMAC. guidelines and to be easy to operate; the drug appeared to have clear clinical effect.
Activities of Daily Living↗
High level processing scope in spoken sentence production.
Five experiments investigate the scope of conceptual and grammatical encoding during spoken sentence production. An online picture description task is employed in which participants generate a variety of sentences in response to an array of moving pictured objects. Experiment 1, demonstrates longer onset latencies for single clause sentences beginning with a complex phrase (e.g. The dog and the kite move above the house) than for matched single clause sentences beginning with a simple phrase (e.g. The dog moves above the kite and the house). This finding suggests that more time is dedicated to the processing of the first phrase of an utterance than the remainder prior to speech onset. Experiments 2 and 3, compare the production of single and double clause sentences. The main effect of Experiment 1 is replicated. However, the data also suggest that some time is dedicated to the processing of elements within the second clause prior to speech onset. In Experiment 4, when participants are allowed to preview pictures prior to movement and timer onset the effect of initial phrase complexity is significantly reduced indicating that the latency effects observed previously primarily reflect lemma access. Finally, Experiment 5 demonstrates that this reduction is greater for nouns within the first phrase than for nouns beyond it. We conclude from these experiments that, prior to speech onset, lemma access is completed for the first phrase of an utterance and that high level processing is initiated but not completed for the remainder of a sentence beyond the first phrase.
Adult↗
Erythroblastic synartesis: an auto-immune dyserythropoiesis.
Erythroblastic synartesis is a rare form of acquired dyserythropoiesis, first described by Breton-Gorius et al in 1973. This syndrome is characterized by the presence of septate-like membrane junctions and "glove finger" invaginations between erythroblasts, which are very tightly linked together. This phenomenon, responsible for ineffective erythropoiesis, leads to an isolated severe anemia with reticulocytopenia. In the following report, we describe 3 new cases of erythroblastic synartesis associated with dysimmunity and monoclonal gammapathy. In all cases, the diagnosis was suggested by characteristic morphological appearance of bone marrow smears, and further confirmed by electron microscopy. Ultrastructural examination of abnormal erythroblast clusters showed that these cells were closely approximated with characteristic intercellular membrane junctions. The pathogenesis of the dyserythropoiesis was modeled in vitro using crossed erythroblast cultures and immunoelectron microscopy: when cultured in the presence of autologous serum, the erythroblasts from the patients displayed synartesis, whereas these disappeared when cultured in normal serum. Moreover, synartesis of normal erythroblasts were induced by the patient IgG fraction. Immunogold labeling showed that the monoclonal IgG were detected in, and restricted to, the synartesis. A discrete monoclonal plasmacytosis was also found in the patient bone marrow. The adhesion receptor CD36 appeared to be concentrated in the junctions, suggesting that it might be involved in the synartesis. These experiments indicated that a monoclonal serum immunoglobulin (IgG in the present cases) directed at erythroblast membrane antigen was responsible for the erythroblast abnormalities. Specific therapy of the underlying lymphoproliferation was followed by complete remission of the anemia in these cases.
Adult↗
Frontal lobe neuronal injury correlates to altered function in FIV-infected cats.
Six cats infected intravenously at 8 weeks of age with feline immunodeficiency virus Maryland isolate (FIV-MD), were evaluated at 8 and 14 months of age (6 months and 12 months postinfection, respectively) with high spatial resolution proton magnetic resonance spectroscopy (MRS) of the frontal cortex. Two separate control cat groups were evaluated at 8 months and 16 months of age. Single voxel two-dimensional high-resolution proton magnetic resonance imaging was performed using the PRESS sequence by selecting a 0.125 ml volume of interest in the medial frontal cortex. A significant reduction in both N-acetylaspartate (NAA) and NAA: choline ratio was found in the FIV 14-month-old group compared with FIV 8-month-old cats, and to the respective age-matched control 16-month-old cats. A negative correlation between NAA and CD4 lymphocyte count was seen in the FIV-14 group only. This group of FIV cats also exhibited a higher proportion of quantitative electroencephalographic relative slow wave activity (RSWA) that correlated to lower NAA content in the frontal cortical voxel. Although peripheral blood proviral load increased over time of infection, no correlation was found between proviral blood or lymph node load and NAA values, CD4 lymphocyte counts, or frontal cortical RSWA. Thus, this study demonstrated that neurologic functional disruption of the frontal cortex correlated strongly with neuronal injury and/or loss in FIV-MD-infected cats independent of peripheral proviral load. The ability to define in vivo neurodegeneration further in this animal model helps in understanding the neuropathogenesis of lentivirus infection, and possibly, a means to follow progression and reversibility during the initial stages of brain infection as therapeutic agents are identified.
Animals↗
WIN 17317-3, a new high-affinity probe for voltage-gated sodium channels.
The iminodihydroquinoline WIN 17317-3 was previously shown to inhibit selectively the voltage-gated potassium channels, K(v)1.3 and K(v)1.4 [Hill, R. J., et al. (1995) Mol. Pharmacol. 48, 98-104; Nguyen, A., et al. (1996) Mol. Pharmacol. 50, 1672-1679]. Since these channels are found in brain, radiolabeled WIN 17317-3 was synthesized to probe neuronal K(v)1 channels. In rat brain synaptic membranes, [(3)H]WIN 17317-3 binds reversibly and saturably to a single class of high-affinity sites (K(d) 2.2 +/- 0.3 nM; B(max) 5.4 +/- 0.2 pmol/mg of protein). However, the interaction of [(3)H]WIN 17317-3 with brain membranes is not sensitive to any of several well-characterized potassium channel ligands. Rather, binding is modulated by numerous structurally unrelated sodium channel effectors (e.g., channel toxins, local anesthetics, antiarrhythmics, and cardiotonics). The potency and rank order of effectiveness of these agents in affecting [(3)H]WIN 17317-3 binding is consistent with their known abilities to modify sodium channel activity. Autoradiograms of rat brain sections indicate that the distribution of [(3)H]WIN 17317-3 binding sites is in excellent agreement with that of sodium channels. Furthermore, WIN 17317-3 inhibits sodium currents in CHO cells stably transfected with the rat brain IIA sodium channel with high affinity (K(i) 9 nM), as well as agonist-stimulated (22)Na uptake in this cell line. WIN 17317-3 interacts similarly with skeletal muscle sodium channels but is a weaker inhibitor of the cardiac sodium channel. Together, these results demonstrate that WIN 17317-3 is a new, high-affinity, subtype-selective ligand for sodium channels and is a potent blocker of brain IIA sodium channels.
Animals↗
Complication after laparoscopic donor nephrectomy: a case report and review.
BACKGROUND: Laparoscopic procedures are gaining acceptance in the treatment of benign and some malignant urologic disorders. Recently, laparoscopic techniques have been applied to transplant surgery and touted as a safe alternative to traditional open techniques. METHODS: We present a patient who developed a complication from laparoscopic donor nephrectomy that required open corrective surgery. RESULTS: A 25-year-old man underwent laparoscopic donor nephrectomy at a large medical center familiar with the operation. There were no operative or early postoperative complications. Within 6 weeks of the operation, the patient developed signs and symptoms of partial small bowel obstruction. Further evaluation revealed an internal hernia in the retroperitoneum at the site of the nephrectomy. This required a second operation to reduce the hernia and close the defect. CONCLUSION: Laparoscopic donor nephrectomy remains an evolving technique that has not stood the test of time. Larger series will eventually reveal whether this is the procedure of choice as compared to traditional open donor nephrectomy.
Adult↗
Phosphoryl oxime inhibition of acetylcholinesterase during oxime reactivation is prevented by edrophonium.
Reactivation of organophosphate (OP)-inhibited acetylcholinesterase (AChE) is a key objective in the treatment of OP poisoning. This study with native, wild-type, and mutant recombinant DNA-expressed AChEs, each inhibited by representative OP compounds, establishes a relationship between edrophonium acceleration of oxime-induced reactivation of OP-AChE conjugates and phosphoryl oxime inhibition of the reactivated enzyme that occurs during reactivation by pyridinium oximes LüH6 and TMB4. No such recurring inhibition could be observed with HI-6 as the reactivator due to the extreme lability of the phosphoryl oximes formed by this oxime. Phosphoryl oximes formed during reactivation of the ethoxy methylphosphonyl-AChE conjugate by LüH6 and TMB4 were isolated for the first time and their structures confirmed by (31)P NMR. However, phosphoryl oximes formed during the reactivation of the diethylphosphoryl-AChE conjugate were not sufficiently stable to be detected by (31)P NMR. The purified ethoxy methylphosphonyl oximes formed during the reactivation of ethoxy methylphosphonyl-AChE conjugate with LüH6 and TMB4 are 10- to 22-fold more potent than MEPQ as inhibitors of AChE and stable for several hours at pH 7.2 in HEPES buffer. Reactivation of both ethoxy methylphosphonyl- and diethylphosphoryl-AChE by these two oximes was accelerated in the presence of rabbit serum paraoxonase, suggesting that organophosphorus hydrolase can hydrolyze phosphoryl oxime formed during the reactivation. Our results emphasize that certain oximes, such as LüH6 and TMB4, if used in the treatment of OP pesticide poisoning may cause prolonged inhibition of AChE due to formation of phosphoryl oximes.
Acetylcholinesterase↗
Role of C3 cleavage in monocyte activation during extracorporeal circulation.
BACKGROUND: We previously demonstrated that inhibiting formation of terminal complement components (C5a and C5b-9) prevents platelet and neutrophil (PMN) but not monocyte activation during simulated extracorporeal circulation (SECC). This study examined whether earlier complement inhibition during SECC, blocking C3a formation, would additionally prevent monocyte activation. METHODS AND RESULTS: SECC was established by recirculating heparinized whole blood from human volunteers on a membrane oxygenator. CAB-2, a chimeric protein constructed from genes encoding the complement regulatory proteins CD46 and CD55, inactivates the C3/C5 convertases and blocks in vitro generation of C3a, C5a, and C5b-9. CAB-2 was used in 4 experiments at a final concentration of 300 micrograms/mL and 4 experiments at 30 micrograms/mL; 4 control runs used vehicle alone. Samples were assayed for C3a and C5b-9, monocyte activation (CD11b upregulation), PMN activation (CD11b upregulation and elastase release), and platelet activation (P-selectin expression and monocyte-platelet conjugate formation). CAB-2 at both doses significantly inhibited formation of C3a and C5b-9 during SECC. High-dose CAB-2 significantly blocked monocyte and PMN CD11b upregulation and PMN elastase release. CAB-2 also inhibited formation of platelet activation-dependent monocyte-platelet conjugates. CONCLUSIONS: Blockade of complement activation early in the common pathway inhibited monocyte CD11b upregulation during SECC, suggesting that early complement components contribute most to monocyte activation during SECC. As expected, PMN and platelet activation were blocked by terminal complement inhibition. This investigation further elucidates the relation between complement and blood cell activation during simulated cardiopulmonary bypass.
Blood Platelets↗
An automated movement assessment panel for upper limb motor functions in rhesus monkeys and humans.
As part of our studies of age-associated changes in motor functions, we have designed an automated movement assessment panel (MAP) to evaluate upper limb and hand movements. Here we describe two versions of the MAP, one for human testing and one for nonhuman primates, and methods for conducting parallel tests in rhesus monkeys and human volunteers. The results are reported from a battery of tests on young adult rhesus monkeys (n = 10, 5-8 years old), young adult human subjects (n = 10, 18-22 years old) and ten aged human subjects (n = 10, 66-68 years old) to demonstrate the capability of the MAP in quantifying arm and hand movement times. The performance times on the two simplest tasks tested were consistent from trial to trial, demonstrating that a stable behavioral baseline could be established for evaluating changes in motor functions over time and assessing treatments for improving motor functions. Motor learning was seen in the more complex movement tasks tested, indicating their usefulness in analyzing this behavior. Finally, age-associated changes in performance times were robustly delineated by the four tasks evaluated in the human subjects.
Adolescent↗
Barriers to improving endodontic care: the views of NHS practitioners.
AIMS: Concerns have been expressed about the technical quality of NHS endodontic treatment. Bringing performance into line with guidelines for good practice needs to be underpinned by an understanding of barriers to compliance. To this end, our research involved an exploratory investigation of the factors influencing the behaviour of general dental practitioners in their practice of endodontics. MATERIALS AND METHODS: Subjects 12 dental practitioners, representative of varying levels of professional experience and status, and of compliance with good practice guidelines. Data collection In-depth interviews, following a topic guide. Analysis Identification, abstraction and charting of major themes. FINDINGS: Informants' responses suggested that general dental practitioners' endodontic practice is influenced by a complex web of factors. A key barrier to high quality treatment is the NHS remuneration scheme. Undergraduate and postgraduate education and training are also highly influential on practice. Dentists reported employing a range of strategies to manage the time-cost tensions imposed by the remuneration system. Perceived deficiencies in the content and delivery of postgraduate training were highlighted by our informants. CONCLUSIONS: There was a perception among our informants that the NHS fee structure needs to be revised. Their views suggest that a system which rewards quality rather than volume may be more appropriate, but, we believe, such a system would need to take into account efficiency as well as effectiveness. Modification of the current system of postgraduate training in endodontics is also indicated by the views expressed in the interviews. From the diversity of views and from a critical review of the literature, we conclude that flexibility is the key note in changing practice, with no single strategy likely to be universally appropriate.
Attitude of Health Personnel↗
Novel 23-base-pair duplication mutation in TSC1 exon 15 in an infant presenting with cardiac rhabdomyomas.
Tuberous sclerosis (TSC) is a dominantly inherited disorder due to mutations at two gene loci, the TSC1 locus on chromosome 9q34 and the TSC2 locus on chromosome 16p13.3. The TSC2 and the TSC1 genes have now been cloned, enabling mutation analysis. We report results of mutation analysis in a sporadic case of TSC first identified in intra-uterine life on the basis of the presence of cardiac rhabdomyomas. Postnatally this infant was also found to have subependymal nodules on brain computed tomographic scan. Hypomelanotic macules were not detected neonatally or at 12 months of age. The specific TSC1 exon 15 mutation found in our patient has not previously been reported in cases of TSC. This mutation involves duplication of a 23-bp segment of DNA between two 9-bp repeated sequence elements within exon 15. These repeat elements are located between nucleotides 1892-1900 and between nucleotides 1915-1923 within the TSC1 gene sequence. It is likely that the presence of these two repeated elements predisposes to misalignment of DNA strands and unequal crossing over. The mechanism of origin of rhabdomyomas in TSC is reviewed. Loss of heterozygosity in the TSC gene regions has been reported in cardiac rhabdomyomas; however, these lesions are self-limiting in their growth. The basis for this self limiting proliferation is not clear. One interesting postulation is that cardiac rhabdomyomas may be due to delay or failure of apoptosis which occurs as part of the normal remodeling process in the heart.
Base Sequence↗