Purple urine bags: a geriatric presentation of lower urinary tract infection.
Explore the source record for details and available documents.
Aged↗
Biomedical subjects
E Martin
Publications and source records attributed to E Martin.
Long term outcome after out-of-hospital cardiac arrest with physician staffed emergency medical services: the Utstein style applied to a midsized urban/suburban area.
OBJECTIVE: To test the effect of a physician staffed advanced cardiac life support (ALS) system on patient outcome following out-of-hospital cardiac arrest. DESIGN: Observational study. SETTING: Two tier basic life support (BLS) and physician staffed ALS services in the midsized urban/suburban area of Heidelberg, Germany. PATIENTS: All patients suffering out-of-hospital cardiac arrest of cardiac aetiology between January 1992 and December 1994 and who were covered by ALS services. INTERVENTIONS: Physician staffed ALS services. MAIN OUTCOME MEASURES: Return of spontaneous circulation, hospital discharge, and one year survival, according to the Utstein style. RESULTS: Of 330 000 inhabitants, 755 suffered from cardiac arrest covered by the Heidelberg ALS services. In 512 patients, cardiopulmonary resuscitation had been initiated. Of 338 patients with cardiac aetiology, return of spontaneous circulation was achieved in 164 patients (49%), 48 (14%) were discharged alive, and 40 (12%) were alive one year later; most of these patients showed good neurological outcome. Thus, 4.85 patients with cardiac aetiology were saved by the ALS services and discharged alive per 100 000 inhabitants a year. Ventricular fibrillation or tachycardia was detected in 106 patients (31%), other cardiac rhythms in 40 (12%), and asystole in 192 (57%). Hospital discharge rates (and one year survival) in these subgroups were 34.0% (29.2%), 12.5% (7.5%), and 3.6% (3.1%), respectively. Discharge rates increased if cardiac arrest was witnessed (bystander, 20.0%; BLS/ALS personnel, 21.4%; non-witnessed arrest, 3.3%; p < 0.01), and if the time period between the alarm and the arrival of the ALS unit was four minutes or less (</= 4 minutes, 30.6%; 4-8 minutes, 10.4%; > 8 minutes, 8. 1%; p < 0.001). In 69 patients with bystander witnessed cardiac arrest with ventricular fibrillation, the discharge rate was 37.7%; 21 patients were alive after one year. CONCLUSIONS: A two tier BLS and physician staffed ALS system is associated with good long term outcome of patients suffering from out-of-hospital cardiac arrest of cardiac aetiology in a midsized urban/suburban area. Further studies, however, are required to assess whether having a physician in the ALS unit is an independent determinant for improved long term outcome.
Aged↗
Concentration changes of malondialdehyde across the cerebral vascular bed and shedding of L-selectin during carotid endarterectomy.
BACKGROUND AND PURPOSE: Oxidative stress has been postulated to account for delayed neuronal death due to ischemia/reperfusion. We investigated cerebral formation of malondialdehyde as an index of lipid peroxidation in relation to different sources of reactive oxygen species in patients undergoing carotid endarterectomy. METHODS: In 25 patients undergoing carotid endarterectomy, jugular venous-arterial concentration differences of brain metabolites, malondialdehyde, plasma total antioxidant status, and soluble P-selectin and L-selectin were measured. A carotid artery shunt (n=5) was placed only after complete loss of somatosensory evoked potentials, indicating a focal cerebral blood flow <15 mL/min per 100 g. RESULTS: As an indication of cerebral lipid peroxidation, jugular venous-arterial malondialdehyde concentration differences were significantly enhanced before reperfusion, and an additional rise was observed 15 minutes after reperfusion. Plasma total antioxidant status significantly decreased during carotid artery occlusion only in patients with carotid artery shunt. This decrease was matched by cerebral formation of adenosine, hypoxanthine, and nitrite/nitrate. While jugular venous-arterial concentration differences of soluble P-selectin showed changes similar to those of malondialdehyde, the concentration difference for soluble L-selectin was enhanced exclusively at 15 minutes after reperfusion. CONCLUSIONS: Short-term incomplete cerebral ischemia/reperfusion significantly enhanced cerebral lipid peroxidation, as indicated by malondialdehyde formation. The generation of reactive oxygen species by xanthine oxidase or nitric oxide metabolism might be involved in the induction of lipid peroxidation. The additional rise in cerebral release of malondialdehyde was found to coincide with a significant activation of polymorphonuclear leukocytes across the cerebral circulation.
Adult↗
Visual processing in infants and children studied using functional MRI.
We studied the development of visual processing in 58 children, ranging from 1 d to 12 y of age (median age 29 mo), using functional magnetic resonance imaging. All but nine children had either been sedated using chloral hydrate (n = 12) or pentobarbital (n = 28). Nine children were studied under a full halothane/ N2O:O2 anesthesia. In the first postnatal month, 30% of the neonates showed a positive blood oxygenation level-dependent (BOLD) contrast signal, whereas, for infants between the ages of 1 mo and 1 y, 27% did so. Thirty-one percent of children between 1 and 6 y of age and 71% of children aged 6 y and above showed a positive BOLD contrast signal change to our visual stimulation paradigm. Besides the usual positive BOLD contrast signal change, we also noted that a large portion of the children measured displayed a negative BOLD contrast signal change. This negative BOLD contrast signal change was observed in 30% of children up to 1 mo of age, in 27% between 1 mo and 1 y of age, in 47% between 1 and 6 y of age, and in 14% of children 6 y and older. In the children in which we observed a negative correlating BOLD contrast signal change, the locus was more anterior and more lateral than the positive BOLD contrast signal, placing it in the secondary visual cortical area. The results indicate that when using functional magnetic resonance imaging on children, the primary visual cortical area does not respond functionally in the same manner as that of the adult until 1.5 y of age. This supports earlier clinical and electrophysiologic findings that different cortical mechanisms seem to contribute to visual perception at different times postnatally.
Adult↗
Biphasic edema after hypoxic-ischemic brain injury in neonatal rats reflects early neuronal and late glial damage.
Magnetic resonance imaging with diffusion- and T2-weighted imaging and 31P magnetic resonance spectroscopy was used to investigate the relationship between development of brain edema and alterations of the brain energy metabolism after hypoxia-ischemia (HI) brain injury in 7-d-old rats. The results were correlated with histologic examinations at various times during recovery up to 5 d. Moderate HI, induced by right common carotid artery ligation and subsequent exposure to 8% O2 for 90 min, produced a cytotoxic edema of 52+/-9% brain volume and depressed the ratio of phosphocreatine to inorganic phosphate from 1.43+/-0.21 to 0.11+/-0.09. Within 1 h of reoxygenation, the edema decreased to 4+/-2% of brain volume, demarcating the core of the lesion. At 5 h of recovery, a secondary cytotoxic edema together with a newly developing vasogenic edema expanded again, reaching its maximal extent of 45+/-10% brain volume at around 24 h. The ratio of phosphocreatine to inorganic phosphate recovered slowly, reaching 1.12+/-0.27 around 13 h. Thereafter it declined again in a manner analogous to the observations made in human newborns after severe perinatal asphyxia, reaching trough values of 0.48+/-0.22 around 24 h after HI. At the cellular level, the vast majority of neuronal death occurred before 15 h. Subsequently, strong glial activation lasted 2-3 d after HI. At 5 d, a cystic infarction of 35+/-12% brain volume was found. We conclude that the biphasic evolution of brain edema and energy metabolism reflects early neuronal and late glial damage in response to moderate HI injury. Therefore, the secondary energy breakdown reflects glial activation and subsequent glial death.
Animals↗
Measurement of the validity of a preschool vision screening program.
OBJECTIVES: The validity (sensitivity and specificity) of a preschool vision screening program was measured over a 3-year period to determine how well strabismus and significant refractive errors could be detected. METHODS: Public health nurses were trained to administer tests of visual acuity, stereoacuity, and ocular alignment. Failure on any test, visual acuity of 6/9 or less, stereoacuity of less than 100 seconds of arc, or an apparent misalignment of the eyes resulted in referral to an eye care practitioner. An age-matched control was also referred. Analysis of practitioner reports used predefined study-based criteria for ocular abnormalities. RESULTS: More than 1100 children were screened each year. The annually calculated prevalence of vision problems ranged between 10.5% and 13.8%. The estimated sensitivity varied from 60.4% to 70.9% (specificity, 69.6% to 79.9%). The yield indicated that a very high percentage of children with vision problems were identified for the first time. CONCLUSIONS: The validity of this screening is comparable to that of other school screenings. The limitations are predictable. Consideration should be given to replacing visual acuity tests with a rapid, objective measure of refractive error and ocular alignment.
Age Factors↗
Selective PCR amplification of functional immunoglobulin light chain from hybridoma containing the aberrant MOPC 21-derived V kappa by PNA-mediated PCR clamping.
Explore the source record for details and available documents.
Animals↗
C1-esterase inhibitor and its effects on endotoxin-induced leukocyte adherence and plasma extravasation in postcapillary venules.
BACKGROUND: C1-esterase inhibitor (C1-INH) has been shown to have beneficial effects in patients with sepsis. However, the microcirculatory effects of C1-INH during sepsis are unknown. This study investigated the influence of C1-INH on leukocyte-endothelial cell adhesion, vascular leakage, and venular microhemodynamics in postcapillary venules of rat mesentery during endotoxemia. METHODS: Thirty-two anesthetized Wistar rats randomly received 1 of 4 treatments: pretreatment with infusion of C1-INH in a concentration of 7.5 U.kg-1 body weight (C1-INH-7.5 group, n = 8) or in a concentration of 15 U.kg-1 body weight (C1-INH-15 group, n = 8) followed by continuous infusion of Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 8) was pretreated with saline solution 30 minutes before LPS infusion. The control group (n = 8) received equivalent amounts of saline infusion. Leukocyte adherence, red blood cell velocity, and vessel diameters in postcapillary venules of rat mesentery were determined every 60 minutes during a period of 120 minutes using in vivo videomicroscopy. Vascular permeability was determined by measuring the extravasation of fluorescence-labeled albumin. Venular wall shear rate was calculated from mean red blood cell velocity and vessel diameter. RESULTS: LPS infusion induced a decrease in venular wall shear rate and an increase in leukocyte adherence and vascular permeability in postcapillary venules of rat mesentery. All microcirculatory disturbances were attenuated by pretreatment with C1-INH, showing no significant difference between the 2 concentrations. CONCLUSIONS: Pretreatment with C1-INH attenuates endotoxin-induced leukocyte adherence and macromolecular leakage in postcapillary venules of rat mesentery, indicating that complement inhibition might be a therapeutic tool in the treatment of sepsis.
Animals↗
Prostate specific antigen variation in patients without clinically evident prostate cancer.
PURPOSE: We address long-term within individual variation of serum prostate specific antigen (PSA) in men without clinical or biopsy evidence of prostate cancer. MATERIALS AND METHODS: We studied 943 men from a prostate cancer screening program with 2 PSA (PSA1 and PSA2) measurements available. A third PSA (PSA3) was obtained from 571 men. Only participants with no clinical evidence of cancer were included in the study. Within individual PSA variability was calculated based on indexes of percent coefficient of variation, ratio difference and PSA velocity. The relationship among these indexes, interval between measurements and number of PSA samples was assessed. RESULTS: Mean interval was 670.4 days between PSA1 and PSA2, and 801.8 days between PSA2 and PSA3 (p<0.001). Mean coefficient of variation was 18% after 2 and 15.7% after 3 PSA measurements. Mean ratio differences were -0.047 ng./ml. for 2 and 0.033 ng./ml. for 3 samples. Mean PSA velocity was -0.128 ng./ml. per year for 2 and -0.055 ng./ml. per year for 3 samples, with 95% confidence intervals of 0.634 and 0.315, respectively. Variability was higher if only 2 PSA measurements were done (p<0.001). No clear relationship was found between individual variability and interval between measurements. CONCLUSIONS: PSA velocity is within normal limits in almost all men (more than 95%) without clinically relevant prostate cancer. PSA individual variability is not fully dependent on the time between measurements when intervals are long, and can be substantially decreased with a third PSA sample.
Aged↗
[Pre-eclampsia and anesthesia].
The management of anaesthesia in patients suffering preeclampsia has to be selected individually. There is a high rate of caesarean sections in patients with preeclampsia. Intubation anaesthesia or regional anaesthesia are commonly used methods and can be considered comparable and equally useful. In our opinion, the application of regional anaesthesia should be preferred, if the initial criteria, such as normal neurologic status and blood coagulation, are fulfilled. We believe in a considerable reduction of vital risks when using regional anaesthesia. Our aim was to figure out the risk-factors of preeclampsia and preterm maturity regarding anaesthesia management. Preeclampsia is a severe illness in pregnancy with a frequency of 5-10%. In 1997, we experienced 73 patients with praeeclampsia according to the definition of ISSPH. Mode of delivery was conventional in 10 patients, 2 patients had a vacuum extraction and 61 patients needed a caesarean section. The rate of epidural anesthesia for delivery was 51%. We used epidural anaesthesia in 6 spontaneous deliveries, in 2 vacuum extractions and in 30 caesarean sections. There were no problems with epidural anaesthesia and the outcome of mother and child was also considered to be excellent. We suggest to use regional anesthesia techniques whenever possible.
Anesthesia, Conduction↗
Influence of C1-esterase inhibitor on tissue oxygenation of jejunal mucosa during endotoxemia.
BACKGROUND: The complement system has been shown to play an important role in the pathogenesis of microcirculatory disturbances in trauma and sepsis. The intestinal mucosa is the most susceptible portion of the gut to impaired perfusion and oxygen delivery. The objective of this study was to investigate the effects of C1-esterase inhibitor (C1-INH) on arterial oxygenation (PaO2) and tissue oxygenation (PtiO2) of jejunal mucosa during endotoxemia. METHODS: Eighteen anesthetized and ventilated rats were laparotomized and a jejunal portion was exteriorized and fixed on a plexiglass stage. The jejunum was punctured and a Clark type microcatheter PO2 probe and a micro thermocouple were placed on the mucosa in order to measure PtiO2. The animals were randomly assigned to receive one of the three treatments: infusion of Escherichia coli lipopolysaccharides (LPS) without C1-INH pretreatment (LPS group); or infusion of LPS with C1-INH pretreatment (C1-INH group); the control group (n = 6) without treatment of either C1-INH or LPS. The mean arterial pressure (MAP), heart rate (HR), PaO2 and PtiO2 were measured at baseline, 60 and 120 min after induction of endotoxemia. RESULTS: Hemodynamic parameters (MAP, HR) in all the three groups showed no significant changes during the study period. PaO2 significantly decreased in the LPS group. This decrease could be attenuated by pretreatment with C1-INH. The mucosal PtiO2 of the jejunum in the control group remained stable. It significantly decreased in the LPS and in the C1-INH groups without showing a significant difference after 120 min of endotoxemia. CONCLUSIONS: Pretreatment with C1-INH was able to diminish a decrease in PaO2 during endotoxemia, indicating that pulmonary injury was attenuated. Endotoxin-induced tissue hypoxia of the intestinal mucosa could not be prevented suggesting a minor involvement of complement activation in this pathophysiological process.
Animals↗
Components of after-hyperpolarization in magnocellular neurones of the rat supraoptic nucleus in vitro.
1. The pharmacological sensitivity of hyperpolarizing components of spike train after-potentials was examined in sixty-one magnocellular neurones of the rat supraoptic nucleus using intracellular recording techniques in a brain slice preparation. 2. In 26 % of all neurones a slow after-hyperpolarization (AHP) was observed in addition to a fast AHP. In 31 % of all neurones a depolarizing after-potential (DAP) was observed. 3. The fast AHP was blocked by apamin whereas the slow AHP was blocked by charybdotoxin (ChTX). The DAP was enhanced by ChTX or a DAP was unmasked if not present during the control period. 4. Low concentrations of TEA (0.15-1.5 mM) induced effects on the slow AHP and the DAP essentially resembling those of ChTX. The same was true for the effects of CoCl2 (1 mM). 5. Spike train after-potentials were not affected by either iberiotoxin (IbTX), a selective high-conductance potassium (BK) channel antagonist, or margatoxin (MgTX), a Kv1.3 alpha-subunit antagonist. 6. Kv1.3 alpha-subunit immunohistochemistry revealed that these units are not expressed in the somato-dendritic region of supraoptic neurones. 7. The effects of ChTX, IbTX, MgTX, TEA, CoCl2 and CdCl2 on spike train after-potentials are interpreted in terms of an induction of the slow AHP by the activation of calcium-dependent potassium channels of intermediate single channel conductance (IK channels). 8. The results suggest that at least the majority of supraoptic magnocellular neurones share the capability of generating both a slow AHP and a DAP. The slow AHP may act to control the expression of the DAP, thus regulating the excitability of magnocellular neurones. The interaction of the slow AHP and the DAP may be important for the control of phasic discharge.
Action Potentials↗
An activity in rat tissues that modifies nitrotyrosine-containing proteins.
Homogenates from rat spleen and lung could modify nitrotyrosine-containing BSA. With incubation, nitrotyrosine-containing BSA lost its epitope to a monoclonal antibody that selectively recognized nitrotyrosine-containing proteins. In the presence of protease inhibitors, the loss of the nitrotyrosine epitope occurred without protein degradation and hydrolysis. This activity was found in supernatant but not particulate fractions of spleen homogenates. The factor was heat labile, was sensitive to trypsin treatment, and was retained after passage through a membrane with a 10-kDa retention. The activity was time- and protein-concentration dependent. The activity increased about 2-fold in spleen extracts with endotoxin (bacterial lipopolysaccharide) treatment of animals, suggesting that the activity is inducible or regulatable. Other nitrotyrosine-containing proteins also served as substrates, while free nitrotyrosine and some endogenous nitrotyrosine-containing proteins in tissue extracts were poor substrates. Although the product and possible cofactors for this reaction have not yet been identified, this activity may be a "nitrotyrosine denitrase" that reverses protein nitration and, thus, decreases peroxynitrite toxicity. This activity was not observed in homogenates from rat liver or kidney, suggesting that there may also be some tissue specificity for the apparent denitrase activity.
Animals↗
p53 mutations in BRCA1-associated familial breast cancer.
Explore the source record for details and available documents.
Breast Neoplasms↗
Cholinesterases in cardiac ganglia and modulation of canine intrinsic cardiac neuronal activity.
Cholinergic neurotransmission plays a significant role in intrinsic cardiac ganglia with the action of acetylcholine being terminated by acetylcholinesterase (AChE, EC 3.1.1.7). Anatomical studies were performed to characterize neurons associated with AChE and a closely related enzyme, butyrylcholinesterase (BuChE, EC 3.1.1.8), in canine intrinsic cardiac ganglia. Histochemical staining for AChE and BuChE in canine right atrial neurons showed that there were four neuronal populations, namely, those that contained AChE only, BuChE only, both AChE and BuChE, and those that did not contain either enzymes. The neuronal activity of intrinsic cardiac neurons in response to substrates and inhibitors of cholinesterases were studied in anesthetized dogs. The activity of intrinsic cardiac neurons, as measured by changes in the number of action potentials, increased by local application of acetylcholine. However, local application of butyrylcholine led to a considerably greater increase in the activity of intrinsic cardiac neurons. In keeping with the neurochemical heterogeneity in intrinsic cardiac ganglia with respect to cholinesterases, the activity generated by most butyrylcholine-sensitive neurons was not influenced by acetylcholine and the activity generated by the most acetylcholine-sensitive neurons was not influenced by butyrylcholine. This suggests that these two agents preferentially influence different populations of intrinsic cardiac neurons. Enzyme kinetic studies demonstrated that canine AChE preferentially catalyzed the hydrolysis of acetylcholine while canine BuChE preferentially catalyzed the hydrolysis of butyrylcholine. Cholinesterase inhibitors Ro 2-1250 and Ro 2-0638 inhibited both canine cholinesterases, while huperzine A preferentially inhibited canine AChE and ethopropazine inhibited canine BuChE. The activity of neurons in the intrinsic cardiac ganglia significantly increased when Ro 2-1250 or Ro 2-0638 was administered locally. The activity of neurons was not affected when huperzine A or ethopropazine was administered, indicating that both cholinesterases must be inhibited to increase neuronal activity. In summary, these data show that in addition to AChE, intrinsic cardiac ganglia also contain distinct populations of neurons that are associated with BuChE, and the activity generated by these neurons is differentially influenced by their substrates. Because simultaneous inhibition of AChE and BuChE leads to increased neuronal activity, it is concluded that AChE- and BuChE-positive intrinsic cardiac neurons may act synergistically to influence the overall tonic activity of intrinsic cardiac ganglia.
Acetylcholine↗
ABO blood group and inhaled nitric oxide in acute respiratory distress syndrome.
Explore the source record for details and available documents.
ABO Blood-Group System↗
Increased ATP production during long-term brain ischemia in rats in the presence of propentofylline.
Forty adult rats were subjected to stepwise two- and four-brain vessel occlusion and propentofylline 25 mg/day per kilogram body weight was intraperitoneally administered for 1 week or 3 weeks. Adenosine 5'-triphosphate, creatine phosphate, adenosine 5'-diphosphate and adenosine were determined in rat parietotemporal cortex by high-pressure liquid chromatography; lactate and pyruvate were measured spectrophotometrically. Stepwise and permanent long-term brain vessel occlusion gradually reduced the concentration of energy-rich phosphates and induced a marked increase in the concentration of adenosine, a parameter of ischemia. Three weeks of propentofylline treatment resulted in a significant increase in cerebral adenosine 5'-triphosphate concentration from 2.16 +/- 0.15 [(-)-propentofylline] to 2.70 +/- 0.24 nmol/mg wet weight during four-vessel occlusion (+25%). This was associated with an enhancement of the adenosine 5'-triphosphate/adenosine 5'-diphosphate ratio (+33%), mainly because of the significant reduction in adenosine 5'-diphosphate concentration. Propentofylline did not prevent the increase in lactate concentration during permanent brain vessel occlusion, but significantly reduced the tissue concentration of adenosine. In summary, the results demonstrate that continuous propentofylline administration over 3 weeks induced a striking increase in rat cortical adenosine 5'-triphosphate concentration during long-term brain vessel occlusion. Thus, propentofylline may have possible neuroprotective effects and could be used in the treatment of patients with chronic cerebrovascular disorders.
Adenosine Triphosphate↗
Inhaled nitric oxide inhibits human platelet aggregation, P-selectin expression, and fibrinogen binding in vitro and in vivo.
BACKGROUND: Recent data suggest that inhaled NO can inhibit platelet aggregation. This study investigates whether inhaled NO affects the expression level and avidity of platelet membrane receptors that mediate platelet adhesion and aggregation. METHODS AND RESULTS: In 30 healthy volunteers, platelet-rich plasma was incubated with an air/5% CO2 mixture containing 0, 100, 450, and 884 ppm inhaled NO. ADP- and collagen-induced platelet aggregation, the membrane expression of P-selectin, and the binding of fibrinogen to the platelet glycoprotein (GP) IIb/IIIa receptor were determined before (t0) and during the 240 minutes of incubation. In addition, eight patients suffering from severe adult respiratory distress syndrome (ARDS) were investigated before and 120 minutes after the beginning of administration of 10 ppm inhaled NO. In vitro, NO led to a dose-dependent inhibition of both ADP-induced (3+/-3% at 884 ppm versus 70+/-6% at 0 ppm after 240 minutes; P<.001) and collagen-induced (13+/-5% versus 62+/-5%; P<.01) platelet aggregation. Furthermore, P-selectin expression (36+/-7% of t0 value; P<.01) and fibrinogen binding (33+/-11%; P<.01) were inhibited. In patients with ARDS, after two who did not respond to NO inhalation with an improvement in oxygenation had been excluded, an increase in plasma cGMP, prolongation of in vitro bleeding time, and inhibition of platelet aggregation and P-selectin expression were observed, and fibrinogen binding was also inhibited (19+/-7% versus 30+/-8%; P<.05). CONCLUSIONS: NO-dependent inhibition of platelet aggregation may be caused by a decrease in fibrinogen binding to the platelet GP IIb/IIIa receptor.
Administration, Inhalation↗