CT-guided decompression of a foreign body obstructing the small bowel.
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Adult↗
Biomedical subjects
B M Taylor
Publications and source records attributed to B M Taylor.
Regulation of the epithelial cell-specific integrin, CD103, by human CD8+ cytolytic T lymphocytes.
BACKGROUND: The destruction of the graft epithelium by CD8+ cytolytic T lymphocytes (CTL) is an important aspect of organ allograft rejection. Our recent finding in a mouse model that the epithelial cell-specific integrin, CD103, defines a subset of CD8+ CTL potentially sheds new light onto such interactions. The goal of the present study was to assess the relevance of these data to the human system. METHODS: CD103 expression by human T-cell populations generated in mixed lymphocyte cultures or isolated from transplant nephrectomy specimens was quantitated using multiparameter FACS analyses. RESULTS: CD103 defined a major subset (26-76%) of CD8+ CTL generated in human mixed lymphocyte cultures; cell sorting experiments confirmed that the CD103+ and CD103- subsets both possess allospecific lytic activity. Anti-transforming growth factor (TGF)-beta blocked the appearance of the CD103+ CTL subset, and persistent expression of CD103 by CD8+ CTL was dependent on bioactive TGF-beta. Isolated CD103+ and CD103- CD8 subsets maintained their phenotypic integrity during in vitro expansion, although optimal CD103 expression on the former was TGF-beta dependent. Although CD103+ cells were rare among activated CD8 cells in peripheral lymphoid compartments (< 10%), analyses of transplant nephrectomy specimens revealed that a major subset (21-61%) of CD8 memory/effector cells that infiltrate rejecting renal allografts express high levels of CD103. CONCLUSIONS: We conclude that CD103 defines a discrete and stable subset of human CD8+ CTL and that CD103 expression by such cells is initiated and maintained by bioactive TGF-beta. These data point to the existence of a human effector subset that is uniquely specialized for the destruction of the graft epithelium.
Animals↗
Local injection of bupivacaine after rubber band ligation of hemorrhoids: prospective, randomized study.
PURPOSE: The aim of this study was to determine if local injection of bupivacaine after hemorrhoidal banding causes a decrease in pain and in the incidence of associated symptoms. METHODS: After hemorrhoidal banding, patients were randomly assigned to receive a local injection of bupivacaine with 1:200,000 epinephrine, an injection of normal saline, or no injection, just superior to each band. Pain was graded by the patient and by the study nurse within 30 minutes, and any associated symptoms were recorded. At intervals 6, 24, and 48 hours postbanding, the patient recorded pain, limitation of activities, and analgesic requirements. Associated symptoms while at home were recorded. RESULTS: Of 115 patients studied, 42 received bupivacaine injection, 42 received normal saline injection, and 31 received no injection. In patients receiving bupivacaine compared with no injection, within 30 minutes postbanding there was a significant reduction in pain graded by the patient (P = 0.000002) and by the nurse (P = 0.000005) and a significant reduction in incidence of nausea (P = 0.01) and shaking (P = 0.008). However, in the bupivacaine group compared with the other two groups, at the intervals of 6, 24, and 48 hours postbanding there was no sustained reduction in the severity of pain and no reduction in analgesic requirements or limitation of normal activities. In the week after banding, there was no difference between groups in symptoms of nausea, shaking, lightheadedness, urinary retention, or bleeding. CONCLUSIONS: Bupivacaine injection may be useful for reducing pain and associated symptoms long enough to tolerate a trip home from the outpatient department but does not show a sustained effect.
Anesthetics, Local↗
Prevention of adhesion formation with use of sodium hyaluronate-based bioresorbable membrane in a rat model of ventral hernia repair with polypropylene mesh--a randomized, controlled study.
BACKGROUND: There is a high incidence of adhesions after ventral hernia repair with polypropylene mesh. Hyaluronic acid (HA)-based membrane has been shown to reduce the incidence of adhesions in the absence of prosthetic mesh. The purpose of this study was to determine the effect of HA membrane on the quantity and grade of adhesions and its effect on strength of repair after abdominal wall repair with polypropylene mesh. METHODS: In 61 rats a full-thickness abdominal wall defect (excluding skin) was created, and a section of small bowel was abraded. The animals were randomized, receiving either HA membrane to cover the viscera or no membrane. The fascial defect was repaired with polypropylene mesh. Equal numbers of animals from each group were killed at 4 weeks and 8 weeks after surgery. Adhesion severity and percentage of mesh surface covered with adhesions were estimated. Tensile strength between mesh and muscle from each animal was measured. Sections of the mesh-muscle interface were examined histologically and measured for thickness and graded for inflammation and fibrosis. RESULTS: Fifty-five animals survived until the end point. Animals in the HA membrane group had a significant reduction in (1) grade of adhesions between small bowel and mesh at 4 weeks (P = .009) and 8 weeks (P = .000001), (2) grade of adhesions between colon and mesh at 8 weeks (P = .00003), and (3) percentage of mesh covered with adhesions at 4 weeks (P = .01) and 8 weeks (P = .0000002). There was no difference between the 2 groups in tensile strength of the repairs, tissue thickness, degree of inflammation, or degree of fibrosis. CONCLUSIONS: HA membrane reduces the quantity and grade of adhesions of both small and large bowel, to polypropylene mesh in a rat model of ventral hernia repair, without compromising strength of the repair.
Animals↗
The effects of kainic acid lesions on locomotor responses to haloperidol and clozapine.
Spontaneous and amphetamine-elicited locomotor activity in rats is reduced by most clinically effective antipsychotic drugs. We have recently demonstrated that intracerebroventricular infusion of kainic acid (KA), which produces cell loss in the hippocampus and other limbic-cortical brain regions, increases spontaneous and amphetamine-elicited locomotion. The present study determined if KA lesions alter the suppressive effects of the antipsychotic drugs, haloperidol and clozapine, on spontaneous and amphetamine-elicited locomotor behavior. Young adult male rats (70 days of age) received intracerebroventricular infusions of vehicle or KA, which produced hippocampal pyramidal cell loss in each rat and more variable cell loss or gliosis in the amygdala, piriform cortex, and laterodorsal thalamus. Thirty days post-surgery, lesioned and control rats were tested once a week for locomotor responses to drug treatments. As observed previously, spontaneous locomotor activity and hyperactivity elicited by amphetamine (1.50 mg/kg s.c.) were greater in lesioned animals than controls. In addition, the level of spontaneous activity and/or amphetamine-elicited hyperlocomotion observed in lesioned rats after haloperidol treatment (0.13, 0.35, or 1.50 mg/kg s.c.) was greater than that found in controls. Locomotor responses to low (6.30 mg/kg) and moderate doses of clozapine (20 mg/kg) were similar in lesioned and control rats, although lesioned rats were more active than controls following the administration of a high dose of clozapine (30 mg/kg). These data indicate that the hyperactivity associated with limbic-cortical lesions may be insensitive to reversal by haloperidol, yet uniquely sensitive to suppression by clozapine.
Amphetamine↗
Analysis of job-share as a process of change.
This paper describes the introduction of a district nursing job-share in a primary health care team. Exploring change theory and different strategies for organizational change, the implications for members of the team are considered. In addition, changes in the balance of power which resulted in conflict within the district nursing team are discussed.
Humans↗
Roles of adhesion molecules ICAM-1 and alpha4 integrin in antigen-induced changes in microvascular permeability associated with lung inflammation in sensitized brown Norway rats.
Increased microvascular permeability and mucosal edema are pathological features of airway inflammation in asthma. In this study, we investigated the characteristics of the edema response occurring in a model of antigen-induced lung inflammation in sensitized brown Norway rats and examined the effects of monoclonal antibodies (mAbs) to adhesion molecules on this response. Ovalbumin (OA) challenge-induced increases in lung permeability were determined by the leakage of 125I-labeled bovine serum albumin (BSA) into the extravascular tissues of the lungs 24 h after challenge in animals intravenously injected (prechallenge) with this tracer. Inflammatory cell infiltration into the alveolar space was determined by bronchoalveolar lavage (BAL). Mean extravascular plasma volume in the lung increased 233% as compared with control (P < 0.005) at 24 h and increased to 517% by 72 h. The 24-h edema response was completely inhibited by two oral doses (0.1 mg/kg) of dexamethasone 1 h before, and 7 h after, challenge. Intraperitoneal administration of the anti-rat ICAM-1 mAb 1A29, or anti-rat alpha4 integrin mAb TA-2 (2 mg/kg at 12 and 1 h before, and 7 h after, antigen challenge), significantly suppressed eosinophil infiltration into the alveolar space without inhibiting the enhanced microvascular leakage and lung edema. Determination of plasma antibody concentrations by ELISA of mouse IgG1 indicated that sufficient concentrations of the appropriate mAb were present to block alpha4- or ICAM-1-dependent adhesion. The results suggest that increases in microvascular permeability and plasma leakage occurred independently of eosinophil accumulation.
Animals↗
Changes in membrane properties during energy depletion-induced cell injury studied with fluorescence microscopy.
The changes in membrane structural properties occurring during the process of ATP depletion-induced cell injury in adherent human astrocytoma cells (UC-11 MG) were studied with two epifluorescence techniques: 1) steady-state fluorescence anisotropy (r) to examine microstructural changes in the membrane phospholipids and 2) fluorescence redistribution after photobleaching (FRAP) to examine membrane fluidity changes. A new method for r measurement was established that provides the unique advantage of simultaneously monitoring both vertical and horizontal polarized fluorescence emissions needed for the calculation of r. In this study, r in the astrocytoma cells labeled with 1-(4-trimethylammonium phenyl)-6-phenyl-1,3,5-hexatriene p-toluenesulfonate was shown to remain stable for up to 90 min. However, when the cells were treated with 75 microM iodoacetic acid (IAA), a metabolic inhibitor that induces rapid depletion of cellular ATP, r continually decreased, indicating a decrease in membrane lipid order and perturbation of the bilayer structure. This decrease in r could be prevented by the pretreatment of cells with lipophilic antioxidants such as tirilazad or gossypol. Tirilazad itself caused a significant increase in r, suggesting that tirilazad intercalates into the membrane bilayer and profoundly increases the lipid order in uninjured cells. Gossypol, however, did not exhibit this property. Further investigations into these phenomena with FRAP confirmed the r results and indicated that membrane fluidity increased while its structure became less rigid during the process of ATP-induced cell injury. In addition, lipophilic antioxidants prevented the membrane structural aberrations induced by IAA. Experimental results suggest that different mechanisms of cytoprotective action may exist for tirilazad and the antioxidant gossypol. Gossypol appears to prevent or delay the observed cell injury entirely because of its antioxidant action, whereas tirilazad's protection is mediated not only via its antioxidant activity, but also by its ability to increase cell membrane lipid order.
Adenosine Triphosphate↗
Alterations in reactive oxygen, pH, and calcium in astrocytoma cells during lethal injury.
Exposure of cultured human astrocytoma cells to iodoacetic acid results in rapid depletion of cellular ATP and cell death. Pathophysiological changes in the injured cells, including formation of reactive oxygen species (ROS), cell viability, glutathione, pH, and cytosolic calcium, were characterized at the cellular level via fluorescence microscopy. After iodoacetic acid treatment, cellular ATP and intracellular glutathione fell sharply to undetectable levels within 2 h. ROS, as detected by the oxidation of dichlorofluorescein, appeared in 20 min and reached a maximum before the loss of membrane integrity. Cells became acidotic within 10 min. Cytosolic free calcium concentration exhibited a slow increase and then a sharp influx shortly before the rupture of the cell membrane. The addition of lipophilic antioxidants, nordihydroguaiaretic acid or the troloxamine U-78517F, eliminated the accumulation of ROS and delayed the onset of cell death without affecting other parameters observed in the early phase of the injury. We conclude that ROS is formed and may play important roles during lethal cell injury caused by energy depletion.
Adenosine Triphosphate↗
Phenotypic analysis of airway eosinophils and lymphocytes in a Th-2-driven murine model of pulmonary inflammation.
In order to investigate whether the pulmonary response to helminth antigens mimics that seen in allergic inflammation of the airways, we have examined the phenotypic characteristics of lymphocytes and eosinophils recruited to the airways following Nippostrongylus brasiliensis (N.b.) infection. Specifically, the cellular response was divided into an early and a late phase. During the early response there was a small but significant increase in neutrophil numbers recovered by bronchoalveolar lavage (BAL). Phenotypic analysis of BAL leukocytes revealed an early rise in the percentage of BAL lymphocytes expressing the naive T cell markers CD45RB and L-selectin, and the activation marker IL-2R. In addition, during the early response, there was an increased percentage of lymphocytes expressing the gamma delta TCR, but not the alpha beta TCR. In contrast, the late response was marked by a much larger accumulation, in the lungs and BAL, of memory CD4+ T lymphocytes and an influx of small, hypodense eosinophils which produced LTB4 and LTC4 on stimulation with calcium ionophore. At this time there was a substantial increase in the number of T lymphocytes and eosinophils expressing ICAM-1 and the integrins VLA-4 and LFA-1, implicating these adhesion molecules in inflammatory cell recruitment to the airways. We conclude that the pattern and phenotypic characteristics of the cellular recruitment seen following N.b. infection resemble those seen in early- and late-phase allergic inflammation of the airways in asthma, and therefore N.b. may be used to model these aspects of the disease.
Animals↗
The mechanism of cytoprotective action of lazaroids I: Inhibition of reactive oxygen species formation and lethal cell injury during periods of energy depletion.
Tirilazad mesylate and related compounds, known as lazaroids, are recognized as inhibitors of membrane lipid peroxidation that also act as free radical scavengers. These compounds have demonstrated protective activity in animal models of traumatic head injury and cerebral ischemia. In this study we used an in vitro cell model to investigate the mechanism by which tirilazed mesylate and related antioxidants delay or prevent the lethal cell injury provoked by chemically induced energy depletion. When the cultured human astrocytoma cell line UC-11MG was treated with the metabolic inhibitor sodium iodoacetate for 4 hr, the cells exhibited signs of irreversible cell injury, including alterations in plasma membrane morphology, the breakdown of membrane phospholipids (release of arachidonic acid into the extracellular medium) and the loss of viability as indicated by the leakage of cytoplasmic components. A large quantity of reactive oxygen species (ROS) was detected in the injured cells by a dichlorofluorescin assay. Increases in early lipid peroxidation products were detected as elevated hydroxyeicosatetraenoic acids in the membrane phospholipds, which indicated that the membrane lipids were oxidatively damaged. The addition of tirilazad mesylate, a troloxamine derivative or the common phenolic antioxidant nordihydroguaiaretic acid effectively prevented the increases in ROS, attenuated the elevation of hydroxyeicosatetraenoic acids, and delayed irreversible cell injury. We propose that the destruction of crucial cell constituents in the lipophilic compartments by ROS is one of the major causes of lethal cell injury. The cyytoprotective action of the lazaroids in related, as least in part, to their ability to block the formation of ROS and to arrest the secondary cell injury.
Arachidonic Acids↗
Recurrent superior mesenteric artery (Wilkie's) syndrome: a case report.
Superior mesenteric artery syndrome (SMAS) is a rare condition. The diagnosis is usually made by exclusion. A previously healthy 20-year-old woman who had recurrent SMAS is described. Diagnosis of the condition was difficult. Initially, small-bowel enteroclysis, upper gastrointestinal series and endoscopy, biopsy of gastric and duodenal mucosa, abdominal computed tomography (CT) and ultrasonography were used to make the diagnosis. Abdominal CT suggested pancreatitis causing compressive obstruction of the superior mesenteric artery. Conservative management was helpful at first, but cramping and projectile emesis recurred. Upper gastrointestinal series suggested duodenal distension and a filling defect in the region of the superior mesenteric artery. Repeat endoscopy showed a lateral pulsatile compression in the region of the distal duodenum and SMAS was diagnosed. Medical therapy was not helpful so duodenojejunostomy was carried out. The operation was successful and the patient was symptom-free for 1 year, when the syndrome recurred, with symptoms of periumbilical pain, intermittent episodes of vomiting and loose stools. At reoperation the duodenojejunal anastomosis was found to be displaced to the left of the superior mesenteric artery pedicle causing recurrent obstruction. The duodenojejunostomy was converted to a Roux-en-Y duodenojejunostomy. The patient has since remained well. A MEDLINE search of the literature for the period 1961 to October 1994 revealed that there were no reported cases of a recurrence of SMAS in an otherwise healthy adult patient. In spite of the difficulty in diagnosing this condition, heightened awareness can lead to early diagnosis and avoid unnecessary suffering for the patient.
Adult↗
Gender-power relations and safer sex negotiation.
This paper examines the gender-power relations in heterosexual relationships and discusses the implications for women in attempting to negotiate safer sex. Whilst acknowledging the need for examining both male and female perceptions of sexuality, the paucity of research on men's heterosexual experiences has restricted this paper to the consideration of the woman's standpoint. Reviewing the literature, the complexities of sexual relationships are explored in terms of the power imbalance which arises from the ideologies of femininity and masculinity. The implications for safer sex promotion by practice nurses working in primary health care teams are then discussed within the context of gender divisions of labour and gender role conflict.
Female↗
Lack of effect of postinjury treatment with methylprednisolone or tirilazad mesylate on the increase in eicosanoid levels in the acutely injured cat spinal cord.
Methylprednisolone (MP) improves motor recovery in spinal cord-injured patients when administered in a 24 h intensive high dose regimen beginning within 8 h after spinal cord injury (SCI). The rationale for this regimen has been based upon the need for high doses (i.e., 30 mg/kg initial IV dose) to inhibit posttraumatic lipid peroxidation (LP) in the injured spinal segment. However, injury also triggers the immediate calcium-mediated activation of phospholipase A2 (PLA2), the release of arachidonic acid, and the enzymatic formation of potentially deleterious prostaglandins (PGE2 alpha, PGE2), thromboxane A2 (TXA2), and leukotrienes (LTs). Thus, in view of the glucocorticoid receptor-mediated inhibition of PLA2 that underlies much of MP's antiinflammatory actions, an additional neuroprotective mechanism may relate to an inhibition of eicosanoid formation. Using the cat spinal cord compression model (180g x 5 min at L3; Na pentobarbitol anesthesia), we examined whether 30 min postinjury dosing with MP (30 mg/kg IV) could attenuate spinal tissue eicosanoid levels measured by enzyme immunoassay at 1 h (Experiment 1). Pial blood flow was measured over the dorsal columns at the injury site using laser doppler flowmetry to monitor posttraumatic hyperperfusion as an index of the microvascular pathophysiology of acute SCI. In vehicle treated animals at 1 h postinjury, there was a significant increase in the tissue levels of PGF2 alpha (+290%), PGE2 (+260%), TXB2 (stable analog of TXA2, +126%), and LTB4 (+73%) in comparison to sham, uninjured animals. However, 6-keto-PGF1 alpha (stable analog of prostacyclin or PGI2) and LTC4 did not increase. Methylprednisolone did not reduce the increase in eicosanoid production. In the case of LTB4 and LTC4, MP actually increased the levels further. In addition, we examined the effects of a double dose MP regimen (30 mg/kg IV at 30 min plus 15 mg/kg IV at 2.5 h postinjury) on spinal cord eicosanoid levels at 4 h postinjury (Experiment 2). At 4 h postinjury, significant increases in PGF2 alpha, PGE2, TXB2, and 6-keto-PGF1 alpha were observed, and with the exception of PGE2, no MP attenuation of the increased eicosanoids was seen. These results fail to provide evidence that postinjury administration of high dose MP exerts a significant anti-PLA2 action. On the other hand, MP effectively inhibited secondary spinal cord pial hyperperfusion, which is believed to be largely mediated by free radical-lipid peroxidative mechanisms. Thus, it seems likely that the protective action of MP on the acute microvascular pathophysiology of SCI is mediated by its well-documented effects on posttraumatic LP.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Generation and detection of hydroxyl radical following experimental head injury.
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Animals↗
Effects of the lipid peroxidation inhibitor tirilazad mesylate (U-74006F) on gerbil brain eicosanoid levels following ischemia and reperfusion.
The present study measured the production of eicosanoids in the gerbil brain during early reperfusion after either a 3-h unilateral carotid occlusion (UCO, model of focal ischemia) or a 10-min bilateral carotid occlusion (BCO, model of global ischemia). Arachidonic acid (AA) metabolites were examined to determine if pretreatment with the 21-aminosteroid lipid peroxidation inhibitor U-74006F (tirilazad mesylate) could influence postreperfusion synthesis of brain eicosanoids. In the 3-h UCO focal ischemia model, there was an early (5-min) postreperfusion elevation in brain levels of PGF2 alpha, TXB2 and LTC4 (P < 0.05 vs. sham for all three eicosanoids). LTB4 also rose but not significantly. On the other hand, PGE2 and 6-keto-PGF1 alpha tended to decrease during ischemia and at 5-min postreperfusion (P < 0.05 vs. sham for PGE2). Pretreatment with known neuroprotective doses of U-74006F in this model (10 mg/kg i.p. 10 min before and again immediately upon reperfusion) did not affect the increase in PGF2 alpha or TXB2 but significantly blunted the elevations in LTC4 and LTB4. The postreperfusion decrease in PGE2 was also attenuated. In the 10-min BCO global ischemia model, there was also an increase in each of the measured eicosanoids, except LTB4, at 5 min after reperfusion. Pretreatment with U-74006F (10 mg/kg i.p. 10 min before ischemia) selectively decreased the rise in LTC4 but did not significantly affect the other eicosanoids. In contrast, the antioxidant actually caused a significant enhancement of the postreperfusion increase in PGE2 vs. vehicle-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Degradation of membrane phospholipids in the cultured human astroglial cell line UC-11MG during ATP depletion.
The exposure of brain cells to adverse conditions, such as ATP depletion, induces the degradation of membrane phospholipids and the accumulation of free fatty acids. We have investigated the mechanism of membrane breakdown in an in vitro cell injury model. Confluent cells from the human astroglial cell line UC-11MG were treated with sodium iodoacetate to deplete their intracellular ATP. Large amounts of saturated (palmitic acid) and unsaturated (oleic, linoleic and arachidonic acid) free fatty acids as well as diacylglycerols containing prelabeled fatty acids were released from the cells prior to the loss of plasma membrane integrity. The capacity of the cells to reincorporate free fatty acid into membrane phospholipids decreased in parallel with the loss of intracellular ATP, indicating the failure of the acyltransferase pathway. The addition of the phospholipase A2 inhibitors manoalide, mepacrine, or U-26384, or the phospholipase C inhibitor U-73122, reduced the severity of cell injury, but did not maintain cell viability. The addition of a battery of protease inhibitors with or without the phospholipase inhibitors had no protective effect. These results suggest that the activation of phospholipases A2 and C coupled with the loss of the reacylation process lead to the breakdown of membrane components during lethal cell injury.
Adenosine Triphosphate↗
Metabolism of leukotriene B4 by guinea pig eosinophils.
The metabolism of leukotriene B4 (5(S),12(R)-dihydroxy-6-cis-8,10-trans-14-cis-eicosatetraenoic acid) by isolated guinea pig eosinophils was investigated. Incubation of guinea pig eosinophils with [3H]-leukotriene B4 resulted in the rapid conversion of leukotriene B4 to several more polar metabolites. Two of these metabolites were identified by ultraviolet spectroscopy and gas chromatography-mass spectrometry as the omega oxidation products 5(S),12(R),20-trihydroxy-6,8,10,14-eicosatetraenoic acid (20-hydroxy-leukotriene B4) and 5(S),12(R),19-trihydroxy-6,8,10,14- eicosatetraenoic acid (19-hydroxy-leukotriene B4). Two novel metabolites, 5(S),12(R),18,19-tetrahydroxy-6,8,10,14 eicosatetraenoic acid (18,19-dihydroxy-leukotriene B4) and 5(S),12(R)-dihydroxy-1,18-dicarboxylic-6,8,10,14,16-octadecapentaenoi c acid (delta 16,17-18-carboxy-19,20-dinor-leukotriene B4) were tentatively identified. The identification of these compounds indicates that guinea pig eosinophils are capable of metabolizing leukotriene B4 by both omega and beta oxidation. This catabolic activity may play a role in modulating inflammatory reactions by removing the chemoattractant leukotriene B4 from inflammatory sites.
Animals↗