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A Lee

Publications and source records attributed to A Lee.

At least 289 records · Page 16Linked to original sources

Viscoelastic Responses of Polyhedral Oligosilsesquioxane Reinforced Epoxy Systems.

The properties of nanostructured plastics are determined by complex relationships between the type and size of the nanoreinforcement, the interface, and the chemical interaction between the nanoreinforcement and the polymeric chain, along with macroscopic processing and microstructural effects. Recently, families of mono- and difunctionalized polyhedral oligomeric silsesquioxane (POSS) macromers bearing epoxide groups have been developed. This paper presents an investigation of the thermal and viscoelastic property enhancements in commonly used model epoxy resins reinforced with monofunctional POSS-epoxy macromers. The glass transitions of these POSS-epoxy nanocomposites were studied using differential scanning calorimetry. Small-strain stress relaxations under uniaxial deformation were examined to provide insight into the time-dependent viscoelastic behavior of these nanocomposites. The POSS-epoxy macromers utilized in this study were monofunctional and hence occupied chain terminus points within the network. Nevertheless, they were effective at hindering the molecular motion of the epoxy network junctions. Thus the glass transition temperature, Tg, was observed to increase with increasing weight fraction of the monofunctional POSS-epoxy. The viscoelastic response at temperatures below Tg was examined and was found to correlate to a stretched exponential relaxation function. Time-aging time-superposition was found to be applicable to the data under all test conditions and for all of the materials used in this study. Surprisingly, the instantaneous modulus was not observed to be affected by incorporation of the POSS nanoreinforcement. This suggests that while POSS cages influence polymer chain motions, including the motion of the molecular junctions, these nanoreinforcements did not participate in the overall deformation of the chains. Experiments performed under identical thermodynamic states, revealed that the molecular level reinforcement provided by the POSS cages also retarded the physical aging process in the glassy state. Therefore, the time required to reach structural equilibrium was longer for samples reinforced with POSS-epoxy than for those of the neat resins.

Journal Article↗

alpha2A-adrenergic receptors in the rat nucleus locus coeruleus: subcellular localization in catecholaminergic dendrites, astrocytes, and presynaptic axon terminals.

To define the anatomic substrates subserving the inhibitory actions of alpha2-adrenergic receptors (alpha2-ARs) in the locus coeruleus (LC), we used dual-label immunoelectron microscopy with antibodies directed against the A-subtype of alpha2-AR (alpha2A-AR) and the catecholamine-synthesizing enzyme tyrosine hydroxylase (TH). Of the profiles containing peroxidase labeling for alpha2A-AR (alpha2A-AR-IR) in the LC (n=735), most were dendrites ( approximately 50%), glial processes ( approximately 30%), and axon terminals ( approximately 15%). alpha2A-AR-IR was also observed in unmyelinated axons and perikarya. Within dendrites, alpha2A-AR-IR was associated with nonsynaptic regions of the plasma membrane and subsurface cisternae. Approximately 60% of dendrites with alpha2A-AR-IR were dually labeled for TH. Fifty percent of the axon terminals contacting alpha2A-AR-immunoreactive dendrites formed asymmetric (excitatory) synaptic contacts. Axon terminals with alpha2A-AR-IR were not dually labeled for TH and generally formed asymmetric synapses with TH-immunoreactive dendrites that contained or lacked alpha2A-AR-IR. Astrocytic processes exhibiting alpha2A-AR-IR were closely apposed to TH-labeled dendrites. These results extend previous ultrastructural observations of alpha2A-ARs in the LC and suggest that the inhibitory actions of norepinephrine and epinephrine in this region may be mediated by postsynaptic alpha2A-ARs on catecholaminergic dendrites and presynaptic alpha2A-ARs on excitatory inputs to catecholaminergic dendrites. In addition, the localization of alpha2A-AR-IR in astrocytic processes apposed to TH-immunoreactive dendrites suggests a role for alpha2A-ARs in functional interactions between catecholaminergic dendrites and neighboring astrocytes.

Adrenergic alpha-Agonists↗

Hippocampal alpha2a-adrenergic receptors are located predominantly presynaptically but are also found postsynaptically and in selective astrocytes.

Alpha-adrenergic receptor, subtype 2A (alpha2A-AR), activation is one of the primary modes of action for norepinephrine (NE) in the rat hippocampal formation. In this study, alpha2A-AR immunoreactivity (alpha2A-AR-I) was localized by light and electron microscopy in the rat hippocampus and dentate gyrus by using a previously characterized antibody to the rat alpha2A-AR. By light microscopy, dense alpha2A-AR-I was observed in the pyramidal and granule cell layers. Diffuse and slightly granular alpha2A-AR-I was found in the neuropil in all other laminae, notably stratum lacunosum-moleculare. Ultrastructurally, alpha2A-AR-I was found in neuronal cytoplasm associated with large multivesicular-like organelles and with clusters adjacent to endoplasmic reticula and/or plasmalemma. The distribution of alpha2A-AR-I in the strata oriens, radiatum, and lacunosum-moleculare of hippocampal CA1 and CA3 regions and in the molecular layer of the dentate gyrus was remarkably similar (n > 2,000 profiles examined): alpha2A-AR-I was found in axons and terminals (approximately 40%), glia (approximately 30%), dendritic spines (approximately 25%), and dendritic shafts (approximately 5%). This mixed pre- and postsynaptic distribution was not seen in the stratum lucidum of the CA3 region and the dentate hilar region, where most alpha2A-AR-I was found in axons (approximately 60%) and glia (approximately 30%). Alpha-2A-AR-labeled axons were small and unmyelinated; labeled terminals usually formed asymmetric synapses on unlabeled spines; and labeled dendritic spines were morphologically similar to pyramidal or granule cells. Dual labeling studies demonstrated that some axons contained alpha2A-AR-I and tyrosine hydroxylase (TH), the catecholaminergic synthesizing enzyme, and that some TH-labeled terminals were in close proximity to alpha2A-AR-labeled spines and glia. These studies demonstrate that hippocampal alpha2A-AR-I is localized (1) presynaptically in both noncatecholaminergic and catecholaminergic terminals, (2) postsynaptically in the dendritic spines of pyramidal and granule cells near catecholaminergic terminals, and (3) in some glial processes. These results suggest several sites for NE to exert its effects on hippocampal alpha2A-ARs.

Animals↗

Ultrastructural evidence for prominent postsynaptic localization of alpha2C-adrenergic receptors in catecholaminergic dendrites in the rat nucleus locus coeruleus.

Alpha-2-adrenergic receptor (alpha2-AR) agonists potently inhibit the activity of noradrenergic neurons of the locus coeruleus (LC), an effect that may be mediated by the A- and/ or C-subtypes of alpha2-AR (alpha2A- and alpha2C-AR). To gain insight into the functional significance of these alpha2-AR subtypes in the LC, we have examined their ultrastructural localization by using subtype-specific antibodies. We recently demonstrated that alpha2A-ARs are localized prominently in axon terminals and catecholaminergic dendrites in the LC. In the present study, we sought to identify the subcellular substrates underlying alpha2C-AR actions in the LC by analyzing the ultrastructural distribution of alpha2C-AR immunoreactivity (alpha2C-AR-IR) in sections that were dually labeled for the catecholamine-synthesizing enzyme tyrosine hydroxylase (TH). Alpha-2C-AR-IR was predominantly localized in dendrites, most of which also contained immunolabeling for TH. Within such dendrites, alpha2C-AR-IR was associated with the plasma membrane and occasionally Golgi cisternae and tubulovesicles. The vast majority of dendrites containing alpha2C-AR-IR received asymmetric (excitatory) contacts from unlabeled axon terminals that often contained dense core vesicles. Alpha-2C-AR-IR was observed in some unmyelinated axons and astrocytic processes that were apposed to TH-immunoreactive dendrites but was rarely associated with axon terminals. These results provide the first ultrastructural evidence that alpha2C-ARs (1) are localized postsynaptically in catecholaminergic neurons of the LC and (2) may be strategically situated to modulate the activation of LC neurons by excitatory inputs.

Animals↗

Structural conservation in prokaryotic and eukaryotic potassium channels.

Toxins from scorpion venom interact with potassium channels. Resin-attached, mutant K+ channels from Streptomyces lividans were used to screen venom from Leiurus quinquestriatus hebraeus, and the toxins that interacted with the channel were rapidly identified by mass spectrometry. One of the toxins, agitoxin2, was further studied by mutagenesis and radioligand binding. The results show that a prokaryotic K+ channel has the same pore structure as eukaryotic K+ channels. This structural conservation, through application of techniques presented here, offers a new approach for K+ channel pharmacology.

Amino Acid Sequence↗

Health-related quality of life in patients served by the Department of Veterans Affairs: results from the Veterans Health Study.

BACKGROUND: The Department of Veterans Affairs Health Care System (VA) is the largest integrated single payer system in the United States. To date, there has been no systematic measurement of health status in the VA. The Veterans Health Study has developed methods to assess patient-based health status in ambulatory populations. OBJECTIVES: To describe the health status of veterans and examine the relationships between their health-related quality of life, age, comorbidity, and socioeconomic and service-connected disability status. METHODS: Participants in the Veterans Health Study, a 2-year longitudinal study, were recruited from a representative sample of patients receiving ambulatory care at 4 VA facilities in the New England region. The Veterans Health Study patients received questionnaires of health status, including the Medical Outcomes Study Short Form 36-Item Health Survey; and a health examination, clinical assessments, and medical history taking. Sixteen hundred sixty-seven patients for whom we conducted baseline assessments are described. RESULTS: The VA outpatients had poor health status scores across all measures of the Medical Outcomes Study Short Form 36-Item Health Survey compared with scores in non-VA populations (at least 50% of 1 SD worse). Striking differences also were found with the sample stratified by age group (20-49 years, 50-64 years, and 65-90 years). For 7 of the 8 scales (role limitations due to physical problems, bodily pain, general health perceptions, vitality, social functioning, role limitations due to emotional problems, and mental health), scores were considerably lower among the younger patients; for the eighth scale (physical function), scores of the young veterans (aged 20-49 years) were almost comparable with the levels in the old veterans (>65 years). The mental health scores of young veterans were substantially worse than all other age groups (P<.001) and scores of screening measures for depression were significantly higher in the youngest age group (51%) compared with the oldest age groups (33% and 16%) (P<.001). CONCLUSIONS: The VA outpatients have substantially worse health status than non-VA populations. Mental health differences between the young and old veterans who use the VA health care system are sharply contrasting; the young veterans are sicker, suggesting substantially higher resource needs. Mental health differences may explain much of the worse health-related quality of life in young veterans. As health care systems continue to undergo a radical transformation, the Department of Veterans Affairs should focus on the provision of mental health services for its younger veteran.

Adult↗

Inhibition of a naturally occurring EGFR oncoprotein by the p185neu ectodomain: implications for subdomain contributions to receptor assembly.

Mutant Epidermal Growth Factor Receptor (EGFR) oncoproteins lacking most of subdomains I and II of the extracellular region, a deletion which includes most of the first of two cysteine-rich sequences, have been observed in multiple human epithelial tumors, including malignant gliomas. These EGFR oncoproteins, designated deltaEGFR or EGFRvIII, confer increased tumorigenicity in vivo and are often coexpressed with full-length EGFR in human tumors. We have expressed an ectodomain-derived, carboxyl-terminal deletion mutant of the p185neu oncogene (T691stop) in human glioblastoma cells coexpressing endogenous EGFR and activated deltaEGFR oncoproteins. The p185neu ectodomain-derived mutant forms heterodimers with deltaEGFR proteins and reduces the phosphotyrosine content and kinase activity of deltaEGFR monomers. As a consequence of T691stop neu expression and surface localization, cell proliferation in conditions of full growth and reduced serum and anchorage-independent growth in soft agar was reduced in glioblastoma cells expressing either endogenous EGFR alone or coexpressing EGFR and elevated levels of deltaEGFRs. T691stop neu mutant receptors abrogate the dramatic growth advantage conferred by deltaEGFR in vivo, suggesting that physical associations primarily between subdomains III and IV of the p185neu and EGFR ectodomains are sufficient to modulate signaling from activated EGFR complexes. Receptor-based inhibitory strategies exploit the thermodynamic preference for erbB ectodomains to heterodimerize, thereby creating erbB receptor assemblies which are defective in signaling and do not internalize. Pharmaceuticals which mimic the p185neu ectodomain may therefore have important therapeutic applications in advanced human malignancies expressing erbB receptors.

Animals↗

Cerebral blood flow and metabolism in patients with chronic liver disease undergoing orthotopic liver transplantation.

Changes in cerebral hemodynamics and metabolism associated with anesthesia and liver transplantation may present particular hazards for patients with cirrhosis. Fifteen patients undergoing liver transplantation were studied, 7 of whom had encephalopathy. Cerebral blood flow (CBF) was measured at the start of surgery, during veno-venous bypass and post reperfusion, using a method based on the Kety-Schmidt method. Cerebral metabolism was assessed by measuring the cerebral metabolic rate for oxygen (CMRO2) and the lactate oxygen index (LOI). The cerebral vascular reactivity to carbon dioxide (CO2) was studied during the preanhepatic and post reperfusion phases. During the preanhepatic period, the median CBF was 44 mL/100 g/min at an arterial carbon dioxide tension (PaCO2) of 3.8 kPa. After reperfusion the CBF increased (P < .02) to 102 mL/100 g/min, the arterial hydrogen ion concentration increased from 39 nmol/L to 53 nmol/L (P < .02) and the jugular venous oxygen saturation from 74% to 89% (P < .02). CBF was similar in patients with and without encephalopathy. The cerebral vascular reactivity to CO2 remained intact, although after reperfusion, the CBF for a given PaCO2 was greater, and the slope of the CBF/CO2 response curve diminished. The CMRO2 was normal in patients without encephalopathy. In the encephalopathic patients, the CMRO2 was low during all stages of transplantation (0.54, 0.86, 1.24 mL/100 g/min, respectively). Patients with encephalopathy may be at increased risk of hypoxemic brain injury during transplantation. To minimize this possibility, more detailed neurological monitoring may be useful.

Adult↗

The effect of N-acetylcysteine on oxygen transport and uptake in patients with fulminant hepatic failure.

We have investigated the effect of N-acetylcysteine on hemodynamic variables, oxygen delivery (DO2), oxygen consumption (VO2), and oxygen extraction in patients with fulminant hepatic failure using independent methods of determining DO2 and VO2, thereby eliminating the effect of mathematical coupling, which may have biased previous studies. In 11 patients with severe fulminant hepatic failure, we documented the hemodynamic effects of N-acetylcysteine during the first 5 hours of a standard infusion regime and simultaneously measured VO2 using a method based on respiratory gas analysis. We related physiological changes to plasma N-acetylcysteine concentrations, and compared this group with 7 patients who received placebo infusions. A variable hemodynamic response to N-acetylcysteine was observed that did not differ significantly in comparison with the placebo group, and did not correlate with plasma drug concentrations. The most significant relationship observed between DO2 and VO2 in any patient predicted a 13-mL x min(-1) x m(-2) increase in VO2 when DO2 increased by 100 mL x min(-1) x m(-2); in 8 patients, VO2 was independent of DO2 over the range observed. In the group that received N-acetylcysteine, a small (mean 6 [SD 6] mL x min(-1) x m[-2]) increase in VO2 occurred in comparison with baseline after 1 hour of infusion (P < .01), but changes were not significantly different from the placebo group and were not sustained. N-Acetylcysteine infusion did not increase oxygen extraction or result in an improvement in whole-blood lactate levels or base excess during the study period. We conclude that N-acetylcysteine infusion does not result in clinically relevant improvements in global VO2, or in clinical markers of tissue hypoxia in patients with severe fulminant hepatic failure.

Acetylcysteine↗

Metformin decreases food consumption and induces weight loss in subjects with obesity with type II non-insulin-dependent diabetes.

Metformin often promotes weight loss in patients with obesity with non-insulin-dependent diabetes mellitus (NIDDM). The mechanism may be attributed to decreased food intake. This study has tested the effect of metformin on satiety and its efficacy in inducing weight loss. Twelve diet-treated NIDDM women with obesity were randomly given two dose levels (850 mg or 1700 mg) of metformin or placebo at 0800 for three consecutive days followed by a meal test on the third day on three occasions using a 3x3 Latin square design. The number of sandwich canapes eaten in three consecutive 10-minute periods beginning at 1400 hours was used to quantitate food intake, and the level of subjective hunger was rated just before the sandwich meal with a linear analogue hunger rating scale at 1400 after a 6-hour fast. The prior administration of metformin produced a reduction in calorie intake after each of the two doses of metformin treatment. The 1700-mg metformin dose had the most marked appetite suppressant action. Similarly, hunger ratings were significantly lowered after metformin, and the effect was most pronounced after the administration of 1700 mg of metformin. To assess the efficacy of metformin in reducing bodyweight, 48 diet-treated NIDDM women with obesity who had failed to lose weight by diet therapy were first placed on a 1200-kcal ADA (American Diabetes Association) diet before being randomized to receive either metformin (850 mg) or placebo twice daily in a double-blind fashion for 24 weeks. A 4-week single-blind placebo lead-in period preceded and a 6-week single-blind placebo period followed the 24-week double-blind treatment period. Subjects treated with metformin continued to lose weight throughout 24 weeks of treatment; their mean maximum weight loss was 8 kg greater than that of the placebo group, with corresponding lower HbA1C and fasting blood glucose levels at the end of the active treatment period. These results indicate that metformin decreases calorie intake in a dose-dependent manner and leads to a reduction in bodyweight in NIDDM patients with obesity.

Adult↗

Pro-inflammatory cytokine release and mediation of the acute phase protein response in fulminant hepatic failure.

OBJECTIVE: To study the relationship between interleukin-6 (IL-6), tumour necrosis factor (TNF) and the acute phase protein C-reactive protein (CRP) in patients with fulminant hepatic failure (FHF) and to investigate the potential of peripheral blood mononuclear cells (PBMC) isolated from these patients to stimulate CRP production by isolated human hepatocytes in vitro. SETTING: Patients with FHF were studied at the time of their admission to the intensive care unit. STUDY DESIGN: Serum TNF and IL-6 were measured in 12 patients with FHF, PBMC from 6 of these patients were then cultured in the presence and absence of lipopolysaccharides (LPS). TNF and IL-6 in serum and supernatants were measured by ELISA. PBMC supernatants were added to isolated human hepatocytes and CRP production was measured. RESULTS: Serum IL-6 (348 +/- 172 pg/ml) and TNF (118.5 +/- 15.5 pg/ml) were elevated compared with healthy controls (not detected) and these observations were matched by elevated serum CRP in patients with FHF (38.9 +/- 7 mg/l). Both the production of IL-6 and TNF by PBMC isolated from patients with FHF and the potential of supernatants from these cells to stimulate CRP production by hepatocytes in vitro was significantly reduced compared with controls. CONCLUSION: Despite the observation that patients with FHF have an elevated hepatic acute phase response, PBMC from patients with FHF have reduced potential to produce IL-6 and TNF and elicit an acute phase response in vitro by the time of patient admission to the intensive care unit. One explanation for this observation is early activation and exhaustion of PBMC in vivo.

Acute-Phase Reaction↗

Negative reexploration for cardiac postoperative bleeding: can it be therapeutic?

BACKGROUND: Reexploration of the mediastinum for bleeding is required in 3% to 7% of patients after cardiac operation, with many proving to have no surgically correctable cause. In spite of a "negative exploration," the bleeding often ceases. We propose the hypothesis that such a negative exploration can be therapeutic by reducing marked fibrinolytic activity in the mediastinal cavity. METHODS: Fibrinolytic activity in shed mediastinal blood was compared with that in the system blood in 5 patients after cardiac operation by measuring fibrinogen, fibrin degradation product, plasminogen activator inhibitor-1, and alpha2-antiplasmin levels. RESULTS: Fibrinolytic activity in mediastinal blood was markedly increased when compared with paired systemic venous blood. This was indicated by the mediastinal blood's lower fibrinogen levels (0.47 versus 1.91 U/mL; p < 0.001), very high levels of fibrin degradation products (1,350 versus 200 ng/mL; p < 0.05), and higher levels of plasminogen activator inhibitor-1 (55.5 versus 28.1 ng/mL; p < 0.005). Decreased levels of alpha2-antiplasmin were also observed in the mediastinum (0.50 versus 0.61 U/mL; p < 0.05). CONCLUSIONS: Our data confirm that fibrinolytic activity can be extremely high in the mediastinum in response to clot formation. This may explain the hemostatic effects of a negative reexploration, where irrigation and the removal of clots may reduce the fibrinolytic process; this may allow the bleeding ends of capillaries and small vessels to thrombose. Decreased levels of alpha2-antiplasmin observed suggest that lysine analogs, such as epsilon-aminocaproic acid, may have a beneficial role when locally delivered into the mediastinum.

Aged↗

Does the method of data collection affect the reporting of depression in the relatives of depressed probands?

BACKGROUND: Data is usually collected from different sources in family studies in depression. We sought to determine what effect different methods of data collection had on the reporting of the lifetime prevalence of depression in the relatives of depressed probands. METHOD: We examined the psychiatric histories of 519 first-degree relatives of a consecutive series of 89 hospitalised depressed probands to ascertain their lifetime prevalence of RDC Major Depression. These data on relatives were obtained either directly with the SADS-L (n = 116), indirectly with the Family History RDC (FH-RDC) (n = 283) or by examining the casenotes of the probands (n = 120). RESULTS: The method of data collection had a marked effect on the reported prevalence of depression, with direct interview being much more sensitive in detecting the less severe forms of the illness. The lifetime prevalence of hospitalised depression in relatives, however, was unaffected by the method of the data collection. Variation in lifetime prevalence of depression between the SADS-L and FH-RDC appeared to be due mainly to differences in the sensitivity of the instrumentation rather than to biases in sampling. CONCLUSION: We confirm that indirect sources of family information have reduced sensitivity for the detection of depression in relatives compared with direct interview. LIMITATIONS: The numbers of relatives directly interviewed were small and the probands represented a severely affected sample which limits the generalisability of the findings. CLINICAL RELEVANCE: Combining data from different methods of collection in family studies is therefore problematic unless a narrow definition of caseness is used (e.g. depression requiring hospitalisation).

Bias↗

Respiratory ultrasonography of human parasternal intercostal muscle in vivo.

The parasternal intercostal muscle (PS) is phasically active during inspiration, but its mechanical function in humans is poorly understood. The aim of this study was to describe PS motion ultrasonographically during respiration. We used a 7.5-MHz curvilinear phased array transducer to obtain ultrasonograms of the second right and left interspace in the sagittal plane, 2-3 cm lateral to the sternum, in 4 seated subjects (3M, 1F), during tidal breathing and at residual volume (RV), functional residual capacity (FRC) and total lung capacity (TLC). Images were recorded on videotape and off-line, digitized, transferred to a workstation, and traced manually to outline the external and pleural borders of the PS muscle in relation to a rectangle bounded by the second and third ribs. To assess PS shape and motion, we measured inter-rib distance (Lics), PS thickness (Tps), and motion of the midpoint of the muscle relative to the midpoint of the reference rectangle (Mps). We also calculated the average radius of curvature of the external and pleural PS borders (Re, Rp) over the mid 50% of Lics, and 1/Re and 1/Rp. During tidal breathing, Mps moved ventrally by 0.42 +/- 0.06 mm (p = 0.001) against the pleural pressure gradient, and 1/Re and 1/Rp decreased by 1.1 x 10(-2) +/- 1.6 x 10(-3) mm-1 and 8.4 x 10(-3) +/- 1.4 x 10(-3) mm-1, respectively (p < 0.001). Lics and Tps did not change (p > 0.19). We conclude that, during inspiration, the PS moves ventrally and straightens, and lung volume, neural activation and pleural pressure influence PS shape and motion. The findings support an intercostal stabilizing function of the PS and suggest a novel mechanism by which the PS may contribute to the inspiratory fall in pleural pressure.

Adult↗

Localization of alpha2C-adrenergic receptor immunoreactivity in catecholaminergic neurons in the rat central nervous system.

Given the importance of alpha2-adrenergic receptors in the regulation of catecholaminergic transmission, we analysed the distribution of immunoreactivity corresponding to the C-subtype of alpha2-adrenergic receptor in central catecholaminergic neurons using double-label immunohistochemistry with antibodies directed against alpha2C-adrenergic receptors and tyrosine hydroxylase. Cells exhibiting both alpha2C-adrenergic receptor and tyrosine hydroxylase immunoreactivity were found in most areas containing catecholaminergic cell groups. However, the percentage of double-labelled cells varied in a region-specific manner. In the medulla, alpha2C-adrenergic receptor immunoreactivity was characteristic of only a minority of cells exhibiting tyrosine hydroxylase immunoreactivity (40-43% in area A1/C1, 27-36% in area A2/C2, 35% in area C3) while a larger percentage of double-labelled cells was observed in the pons (65% in A5, 92% in locus coeruleus, 68% in A7). In the midbrain, alpha2C-adrenergic receptor immunoreactivity was detected in most tyrosine hydroxylase-immunoreactive cells in dopaminergic regions (63% in the retrorubral field, 77-83% in substantia nigra, 67% in ventral tegmental area). These results suggest that alpha2C-adrenergic receptors may act as autoreceptors on some central adrenergic and noradrenergic neurons. In addition, the colocalization of alpha2C-adrenergic receptor and tyrosine hydroxylase immunoreactivity in dopaminergic cell groups suggests that reported effects of alpha2-adrenergic receptor agonists in these areas may be mediated by the C-subtype.

Animals↗

Helical CT angiography in the preoperative evaluation of carotid artery stenosis.

PURPOSE: To determine the utility and accuracy of helical CT angiography (CTA) in the evaluation of carotid artery stenosis. METHODS: A comparison of CTA and conventional arteriogram was performed in 53 patients undergoing evaluation for carotid artery stenosis. Ninety-six carotid systems were evaluable. CTA stenosis was determined by the percent of area reduction seen on axial images through the level of greatest narrowing. MIP images were used to identify the point of maximal stenosis and to visualize overall vascular anatomy. The percent diameter stenosis was measured on conventional arteriograms using strict North American Symptomatic Carotid Endarterectomy Trial (NASCET) and European Carotid Surgery Trial (ECST) criteria. RESULTS: Significant correlation was found between CTA and arteriography (NASCET method R=0.87, ECST method R=0.87, p < 0.001). Using NASCET >60% as an indicator for disease, CTA had a sensitivity of 87%, specificity of 90%, accuracy of 89%, negative predictive value of 88%, and positive predictive value of 89%. CTA identified plaque characteristics such as ulcerations (8), occlusion (10), fatty plaques (22), calcifications (48), and fibrosis (2). CTA underestimated 2 cases of short segment stenoses because of volume averaging, but this discrepancy was detected by duplex scan. No complications or renal dysfunction occurred with CTA; 1 patient became symptomatic during arteriography, necessitating termination of the procedure. CONCLUSION: CTA is a safe, non-invasive technique that precisely measures carotid artery area reduction and highly correlates to conventional arteriography. With this new technology, the current standards for carotid artery imaging may need to be reevaluated, and the precise role for helical CTA more clearly defined.

Aged↗