[Fungal contamination of eyedrops].
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Biomedical subjects
Publications and source records attributed to Y Ding.
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The DNA contents of 30 lung cancers were correlated with preoperative chest CT findings. Tumors with diameters less than 4 cm had lower DNA contents than larger ones, and tumors with spiculated margins had lower DNA than those with lobulated or smooth margins. As DNA contents are correlated with prognosis, the border configuration of peripheral lung cancers may be enough to predict prognosis.
STUDY OBJECTIVE: To compare the intraoperative conditions and postoperative recovery of patients following the use of either propofol-nitrous oxide (N2O) or enflurane-N2O for maintenance of outpatient anesthesia. DESIGN: Randomized, single-blind study. SETTING: University hospital outpatient surgery center. PATIENTS: 61 ASA physical status I and II, healthy female outpatients undergoing laparoscopic surgery. INTERVENTIONS: Patients were randomly assigned to one of three anesthetic regimens. Group 1 (control) received thiopental sodium 4 mg/kg intravenously (i.v.), followed by 0.5% to 1.5% enflurane and 67% N2O in oxygen (O2). Group 2 received propofol 2 mg/kg i.v., followed by 0.5% to 1.5% enflurane and 67% N2O in O2. Group 3 received propofol 2 mg/kg i.v., followed by propofol 50 to 160 micrograms/kg/min i.v. and 67% N2O in O2. All patients received succinylcholine 1 mg/kg i.v. to facilitate tracheal intubation and atracurium 10 to 20 mg i.v. to provide adequate relaxation during the maintenance period. MEASUREMENTS AND MAIN RESULTS: Recovery from anesthesia was assessed by a research nurse who was unaware of the anesthetic technique used. The mean +/- SD time to eye opening was significantly longer in the thiopental-enflurane-N2O group (Group 1) than in the propofol-propofol-N2O group (Group 3) (6.1 +/- 2.5 minutes vs. 3.5 +/- 2.8 minutes, respectively). In addition, the mean time to respond to verbal commands was significantly shorter in the propofol induction groups compared with the thiopental induction group. However, the use of enflurane versus propofol for maintenance of anesthesia did not significantly prolong the time from arrival in the recovery room to sitting, tolerating oral fluids, walking, or being judged "fit for discharge." There were no differences among the three groups with respect to postoperative pain or analgesic requirements. Finally, patients who received enflurane for maintenance of anesthesia had a significantly higher frequency of nausea and vomiting than the propofol maintenance group. CONCLUSION: Induction of anesthesia with propofol is associated with a more rapid emergence from anesthesia than induction with thiopental. Maintenance of anesthesia with enflurane did not prolong recovery compared with maintenance with propofol, but enflurane was associated with increased frequency of postoperative nausea and vomiting.
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The lateral geniculate nucleus (LGN) of primates contains three classes of relay cells, the magnocellular (M), parvocellular (P), and koniocellular (K) cells. At present, very little is known about either the structure or function of the K relay cells in New or Old World monkeys (simian primates). In monkeys, K cells are located between the main LGN layers and adjacent to the optic tract. For convenience, these intercalated cell layers are numbered K1-K4 starting closest to the optic tract with K1. The objective of this study was to examine the details of K axon morphology in the primary visual cortex (V1) of owl monkeys and to determine if different K layers give rise to distinct axon types. For this purpose, injections of WGA-HRP or PHA-L were made into specific K LGN layers and the distribution and morphology of the resulting labeled axons were analyzed. Injections of fluorescent tracers also were made within the superficial layers of V1 to further document connections via analysis of the patterns of retrogradely labeled cells in the LGN. Our main finding is that K axons in owl monkeys terminate as delicate focused arbors within single cytochrome oxidase (CO) blob columns in cortical layer III and within cortical layer I. Overall, the morphology of the K axons in these monkeys is quite similar to what we described previously for K geniculocortical axons in the distantly related bush baby (prosimian primate), suggesting that the basic features of this pathway are common to all primates. Our results also provide evidence that the axon arbors from different K layers are morphologically distinct; axons from LGN layer K1 project mainly to cortical layer I, while axons from LGN layer K3 chiefly terminate in cortical layer III. Taken together, these results imply that the basic features of axons within the K pathway are conserved across primates, and that the K axons from different K layers are likely to differ in function based upon their different morphologies.
How neurons in the primary visual cortex (V1) of primates process parallel inputs from the magnocellular (M) and parvocellular (P) layers of the lateral geniculate nucleus (LGN) is not completely understood. To investigate whether signals from the two pathways are integrated in the cortex, we recorded contrast-response functions (CRFs) from 20 bush baby V1 neurons before, during, and after pharmacologically inactivating neural activity in either the contralateral LGN M or P layers. Inactivating the M layer reduced the responses of V1 neurons (n = 10) to all stimulus contrasts and significantly elevated (t = 8.15, P < 0.01) their average contrast threshold from 8.04 (+/- 4.1)% contrast to 22.46 (+/- 6.28)% contrast. M layer inactivation also significantly reduced (t = 4.06, P < 0.01) the average peak response amplitude. Inactivating the P layer did not elevate the average contrast threshold of V1 neurons (n = 10), but significantly reduced (t = 4.34, P < 0.01) their average peak response amplitude. These data demonstrate that input from the M pathway can account for the responses of V1 neurons to low stimulus contrasts and also contributes to responses to high stimulus contrasts. The P pathway appears to influence mainly the responses of V1 neurons to high stimulus contrasts. None of the cells in our sample, which included cells in all output layers of V1, appeared to receive input from only one pathway. These findings support the view that many V1 neurons integrate information about stimulus contrast carried by the LGN M and P pathways.
We determined the effect of relaxation therapy for hypertension in patients whose blood pressure remained elevated despite the use of antihypertensive medication. The effect was assessed in multiple settings, including the relaxation therapist's office, the Hypertension Clinic, and the patient's natural environment, the latter using 24-hour automated ambulatory blood pressure measures. Nineteen patients were randomized either to temperature biofeedback-assisted relaxation or to an attention control, "stress education." Antihypertensive medication was kept constant. In the behavioral therapist's office, blood pressure decreased in equivalent amounts with both treatments. Hypertension Clinic nurse blood pressure remained stable or increased with both treatments, but again there was no difference between treatments. Ambulatory blood pressure increased with relaxation therapy and decreased with stress education, the effect being significant for diastolic pressure. The effects on ambulatory blood pressure were limited to the waking hours. The only variable that showed superior effects for relaxation therapy was physician-determined blood pressure. These results call into question the generalizability of the effects of relaxation therapy from one setting to another.
BACKGROUND: The relation between mood or emotions and concurrent ambulatory blood pressure responses holds both fundamental and clinical interest. METHODS: The primary sample consisted of 69 normotensive or borderline hypertensive but otherwise healthy adult males. The validation sample consisted of 85 healthy male undergraduate college students. Both samples underwent half-hourly 24-hour ambulatory blood pressure measurements on four separate workdays, 1 week apart. At each ambulatory measurement, subjects recorded their behavior, environment, and mood. The circular mood scale, a circular visual analogue scale based on the circumplex model of mood, was used to reflect the totality of a participant's affective state space. Longitudinal random effects regression models were applied in the data analysis. RESULTS: The results for both samples were quite similar. Sleep and posture had the greatest influence on ambulatory blood pressure and heart rate. The effects of the environmental setting, social setting, and consumption were modest but statistically significant. Independent of these covariates, mood exerted a significant effect on blood pressure and heart rate. Relative to the "mellow" default category, blood pressure increased both for "anxious/annoyed" and "elated/happy" and decreased during "disengaged/sleepy" mood. The range of mood-related blood pressure estimates was 6.0/3.7 mm Hg. CONCLUSIONS: The pattern of blood pressure responses suggests that they were related to the degree of engagement of a mood rather than the degree of unpleasantness. The hypothesis that posits that negative affect-related cardiovascular reactivity mediates the observed correlation between negative affect and disease risk should be reconsidered.
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Epithelial ovarian tumors are the most common subtype of ovarian cancer. In this study, we reveal distinct expression signatures of previously uncharacterized ovarian carcinoma subtypes, including endometrioid component of mixed ovarian tumor and Sertoli-Leydig tumor. Both subtypes were compared to the most common and well-characterized ovarian epithelial carcinoma of the serous type. These comparisons were performed by complementaryDNA (cDNA) microarrays allowing high-fidelity measurements of the expression levels of 39,360 human individual cDNA species representing both known and unknown human genes. Functional analysis of differentially expressed genes in Sertoli-Leydig tumor revealed an upregulation in sonic hedgehog pathway, deregulation of several metabolic pathways especially in amino acid metabolism and overexpression of genes associated with protein synthesis, including ribosomal genes.
The purpose of the present study was to investigate bone changes in the adult rat exposed to low lead levels during intake of normal dietary calcium and to contrast these findings with data from our earlier studies performed with animals receiving low dietary calcium concurrent with lead exposure. The present study exposed adult rats to 100 ppm lead via drinking water for 12 weeks and assessed bone histology, 1,25-dihydroxyvitamin D, 25(OH)vitamin D and parathyroid hormone levels. No osteopenia was evident by quantitative bone histology, and circulating levels of 1,25-dihydroxyvitamin D, 25(OH) vitamin D and parathyroid hormone were normal. Bone ash findings documented incorporation of significant amounts of lead into bone mineral. These findings document absence of interference with vitamin D metabolism, absence of secondary hyperparathyroidism and absence of osteopenia following 12 weeks of low lead exposure in the adult rat maintained on normal calcium intake. Results stress the importance of adequate calcium intake in our elderly population who may be exposed to cumulative, low-level lead exposure.
Cognitive-motor functioning or motor skill learning is impaired in humans following traumatic brain injury. A more complete understanding of the mechanisms involved in disorders of motor skill learning is essential for any effective rehabilitation. The specific goals of this study were to examine motor learning disorders, and their relationship to pathological changes in adult rats with mild to moderate closed head injury. Motor learning deficits were determined by comparing the ability to complete a series of complex motor learning tasks with simple motor activity. The extent of neuronal damage was determined using silver impregnation. At all post-injury time points (day 1 to day 14), statistically significant deficits were observed in parallel bar traversing, foot placing, ladder climbing, and rope climbing. Performance improved with time, but never reached control levels. In contrast, no deficits were found in simple motor activity skills tested with beam balance and runway traverse. Histologically, axonal degeneration was widely distributed in several brain areas that relate to motor learning, including the white matter of sensorimotor cortex, corpus callosum, striatum, thalamus and cerebellum. Additionally, severely damaged axons were observed in the primary visual pathway, including the optic chiasm, optic tract, lateral geniculate nuclei, and superior colliculus. These findings suggest that motor learning deficits could be detected in mild or moderate brain injury, and this deficit could be attributed to a diffuse axonal injury distributed both in the motor and the visual systems.
We have previously demonstrated that a 12 kD hypertension-associated protein (HAP) is elevated in essential hypertension and that this protein has the characteristics of natriuresis, inhibition of Na-K-ATPase, displaces 3H-ouabain from binding sites, and is vasoconstrictive in vitro. In the present study, plasma from 101 patients were examined [25 normals (N) age 50, 7 with acute congestive heart failure (CHF), 24 with chronic renal failure (CRF), on dialysis, 5 with idiopathic hyperaldosteronism (PA) and 27 with essential hypertension, untreated (EHT)]. Plasma was extracted with 32% acetonitrile, then analyzed by DELFIA for marinobufagenin and ouabain. In addition, from 32 patients (6 N <50, 6 N >50, 5 CHF, 5 CRF, 6 EHT, and 4 PA) SDS gradient gels were obtained. The 12 kD bands were extracted, analyzed for Na-K-ATPase inhibition, marinobufagenin and ouabain, and compared to 14 kD and 21 kD bands. Marinobufagenin was found to be elevated in CRF, EHT, PA and CHF. Ouabain was increased only in PA. When the relative optical densities of the 12 kD and 21 kD bands were contrasted, CRF, PA, and EHT were found to be increased and CHF to be decreased in the 12 kD band, with no discernible changes in the 21 kD bands. Following extraction of the bands, Na-K-ATPase inhibitory activity measured 38% in 18 pooled 12 kD bands, with essentially no activity found in the 14 kD or 21 kD bands. Thus only the 12 kD HAP band possessed all of the attributes of natriuretic hormone.
By using an antibody to a specific mucus polypeptide (34 kDa) to study whole cell extracts of both a secretory mutant (SB281) and wild type (wt) Tetrahymena, we demonstrate that a 57-kDa polypeptide is a probable precursor to the 34-kDa secretory polypeptide. We postulate that the precursor accumulates in the mutant cells because it cannot be cleaved. This mutant contains no recognizable mature secretory granules (mucocysts). By immunoelectron microscopy, the 34-kDa polypeptide was localized in wt cells specifically to the mature mucocysts and to their released products. Localization in mutant cells occurred in two different types of cytoplasmic vesicles: small electron dense vesicles (0.3-0.5 microns in diameter) and large electron lucent vacuoles (1.2-3.5 microns in diameter). Immunoblot analyses of homogenates of mutant and wt cells with the anti-34-kDa serum revealed a dominant band in the mutant at Mr 57 kDa whereas the wt showed a dominant band only at Mr 34 kDa. Furthermore, the 57-kDa polypeptide is immunoprecipitated with anti-34-kDa serum from the mutant cell. Further evidence for a precursor relation of the 57-kDa polypeptide in mutant cells to the 34-kDa mucus polypeptide of wt cells was obtained by the use of drugs (monensin, chloroquine, NH4Cl) that block secretory product processing in wt cells. Extracts of drug-treated wt cells showed the presence of a 57-kDa cross reacting band even after 18 h of incubation in growth medium whereas untreated control cells contained the 34-kDa mature protein almost exclusively. These results indicate that processing of the precursor to the 34-kDa polypeptide occurs in an acidic compartment(s) possibly in either the trans Golgi network, or condensing vacuoles or both.
BACKGROUND: Recently, it was found that ganglioside GM3, known as a potent monocytic cell differentiation inducer, mimicked bacterial lipopolysaccharide (LPS) in the activation of macrophage-mediated tumor cytotoxicity (MTC). Since GM3 and LPS share partial structural and functional similarity, we postulate that the GM3-induced MTC was due to the induction of nitric oxide(NO) production in murine peritoneal macrophages (M phi s). MATERIALS RESULTS, CONCLUSIONS: Ganglioside GM3 was highly purified from canine erythrocytes by the authors. Murine peritoneal M phi s were used as the effector cells, and mouse ascites hepatoma cell line HCa-F25/16A3-F as the target cells. We found that: GM3 induced NO production by macrophages in a time- and dose-dependent manner; GM3 and IFN-gamma synergistically increased NO production; GM3 markedly enhanced MTC; both NO production and MTC were significantly inhibited by aminoguanidine. These results demonstrated for the first time that ganglioside GM3 in vitro induces the production of nitric oxide by macrophages, and the GM3-induced MTC is NO-dependent.