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At least 703 records · Page 39Linked to original sources
PubMed1984

Metastatic carcinoma of the iris simulating iridocyclitis.

A 46-year-old woman with a history of breast carcinoma and no known metastatic disease presented with iridocyclitis and secondary glaucoma. Intraocular inflammation and pressure elevation persisted despite standard medical therapy, and paracentesis was performed. Cytological examination of the aspirate revealed adenocarcinoma. Subsequent studies disclosed no evidence of extraocular metastasis. Two courses of radiation therapy to the involved eye resulted in a dramatic reduction in intraocular inflammation and allowed temporary control of the intraocular pressure. Ultimately, however, progressive glaucoma necessitated enucleation. This case confirms previous statements that iridocyclitis may be the initial clinical manifestation of metastatic malignancy. In addition, this report emphasises the importance of paracentesis in the diagnostic evaluation of selected cases of anterior uveitis of unknown aetiology.

Adenocarcinoma↗
PubMed1984

Uveal melanoma: case report of extension through the optic nerve to the surgical margin in the orbital apex.

An unsuspected uveal melanoma arising in a phthisical eye extended through the optic nerve to the surgical margin in the orbital apex without involvement of other orbital structures. Step sections showed the continuous extension through the nerve. Factors likely to predispose to optic nerve extension include epithelioid cell type, large tumour size, peripapillary involvement, and glaucoma. Optic nerve extension carries the risks noted with orbital extension of intraocular tumour, but may in addition lead more directly to intracranial invasion, including a chiasmal syndrome. The role of exenteration and radiotherapy in these cases remains uncertain.

Humans↗
PubMed2000

The specific regulation of immune responses by CD8+ T cells restricted by the MHC class Ib molecule, Qa-1.

Over the last three decades considerable evidence has accumulated that CD8(+) T cells regulate peripheral immune responses, in part, by specifically controlling the outgrowth of antigen-triggered CD4(+) T cells. This regulatory function of CD8(+) T cells has been shown, in vivo, to control the emergence of autoreactive CD4(+) T cells as well as CD4(+) T cells reactive to conventional antigens, including alloantigens. In this review, we summarize the evidence that this immune suppression mediated by CD8(+) T cells is dependent, in part, on specific cognate interactions between MHC class I-restricted regulatory CD8(+) cells and antigen-activated CD4(+) T cells. Moreover, we review the evidence that regulatory CD8(+) T cells recognize antigen-activated CD4(+) T cells in a TCR specific manner restricted by the MHC class Ib molecule, Qa-1. The Qa-1 molecule may be uniquely qualified to serve this MHC restrictive function because, unlike conventional MHC molecules, it is preferentially and transiently expressed on activated and not resting CD4(+) T cells. This may assure that only recently antigen-activated CD4(+) T cells expressing Qa-1/TCR peptide complexes will induce regulatory CD8(+) T cells and subsequently become susceptible to regulation. Because Qa-1 also binds to self Qdm peptides that trigger NK (CD94/ NKG2) receptors on CD8(+) T cells, the machinery for homeostatic regulation of regulatory CD8(+) T cells can be envisioned. Finally, we propose a model by which these TCR specific, Qa-1-restricted regulatory CD8(+) T cells selectively downregulate antigen-activated T cells expressing TCRs of certain affinities. Ultimately these regulatory CD8(+) T cells control the peripheral TCR repertoire during the course of immune responses to both self and foreign antigens.

Animals↗
PubMed1998

Glutamate transport and cellular glutamine metabolism: regulation in LLC-PK1 vs. LLC-PK1-F+ cell lines.

The glutamate (Glu) transporter may modulate cellular glutamine (Gln) metabolism by regulating both the rates of hydrolysis and subsequent conversion of Glu to alpha-ketoglutarate and NH+4. By delivering Glu, a competitive inhibitor of Gln for the phosphate-dependent glutaminase (PDG) as well as an acid-load activator of glutamate dehydrogenase (GDH) flux, the transporter may effectively substitute extracellularly generated Glu from the gamma-glutamyltransferase for that derived intracellularly from Gln. We tested this hypothesis in two closely related porcine kidney cell lines, LLC-PK1 and LLC-PK1-F+, the latter selected to grow in the absence of glucose, relying on Gln as their sole energy source. Both cell lines exhibited PDG suppression as the result of Glu uptake while disrupting the extracellular L-Glu uptake, with D-aspartate-accelerated intracellular Glu formation coupled primarily to the ammoniagenic pathway (GDH). Conversely, enhancing the extracellular Glu formation with p-aminohippurate and Glu uptake suppressed intracellular Gln hydrolysis while NH+4 formation from Glu increased. Thus these results are consistent with the transporter's dual role in modulating both PDG and GDH flux. Interestingly, PDG flux was actually higher in the Gln-adapted LLC-PK1-F+ cell line because of a two- to threefold enhancement in Gln uptake despite greater Glu uptake than in the parental LLC-PK1 cells, revealing the importance of both Glu and Gln transport in the modulation of PDG flux. Nevertheless, when studied at physiological Gln concentration, PDG flux falls under tight Glu transporter control as Gln uptake decreases, suggesting that cellular Gln metabolism may indeed be under Glu transporter control in vivo.

ATP-Binding Cassette Transporters↗
PubMed1975

Influence of cardiac neural inputs on rhythmic variations of heart period in the cat.

Spectral analysis was used to investigate variations of heart period in 13 decerebrate cats under different conditions of neural input to the heart. Spectral density plots in intact animals showed three well-defined peaks: P1 (1.5-2.5 cycles/min), P2 (6-10 cycles/min), and P2 (respiratory frequency). In the presence of sympathetic input only the amplitudes of all peaks were decreased; when only vagal input was present the amplitudes of P1 and P2 were increased and there was no change in P3; when neither sympathetic nor vagal input was present the amplitudes of all peaks were decreased. In addition, the amplitudes of P1 and P2 were increased and there was no change in P3; when neither sympathetic nor vagal input was present the amplitudes of all peaks were decreased. In addition, the amplitudes of P1 and P2 were found to be significantly correlated with the mean heart period under the condition of vagal control only. It is concluded that P3 is related to sinus arrhythmia and that P1 and P2 may be related to spontaneous rhythms that are an intrinsic feature of the dynamic regulation of heart period by the vagus system. Sympathetic activity plays no role in the genesis of these rhythms.

Analysis of Variance↗
PubMed2005

Surfactant alterations in acute inflammatory lung injury from aspiration of acid and gastric particulates.

This study examines surfactant dysfunction in rats with inflammatory lung injury from intratracheal instillation of hydrochloric acid (ACID, pH 1.25), small nonacidified gastric particles (SNAP), or combined acid and small gastric particles (CASP). Rats given CASP had the most severe lung injury at 6, 24, and 48 h based on decreases in arterial oxygenation and increases in erythrocytes, total leukocytes, neutrophils, total protein, and albumin in bronchoalveolar lavage (BAL). The content of large surfactant aggregates in BAL was reduced in all forms of aspiration injury, but decreases were greatest in rats given CASP. Large aggregates from aspiration-injured rats also had decreased levels of phosphatidylcholine (PC) and increased levels of lyso-PC and total protein compared with saline controls (abnormalities for CASP were greater than for SNAP or ACID alone). The surface tension-lowering ability of large surfactant aggregates on a bubble surfactometer was impaired in rats with aspiration injury at 6, 24, and 48 h, with the largest activity reductions found in animals given CASP. There were strong statistical correlations between surfactant dysfunction (increased minimum surface tension and reduced large aggregate content) and the severity of lung injury based on arterial oxygenation and levels of albumin, protein, and erythrocytes in BAL (P < 0.0001). Surfactant dysfunction also correlated strongly with reduced lung volumes during inflation and deflation (P = 0.0004-0.005). These results indicate that surfactant abnormalities are functionally important in gastric aspiration lung injury and contribute significantly to the increased severity of injury found in CASP compared with ACID or SNAP alone.

Acute Disease↗
PubMed2006

Pneumocystis carinii infection sensitizes lung to radiation-induced injury after syngeneic marrow transplantation: role of CD4+ T cells.

A murine model of bone marrow transplant (BMT)-related lung injury was developed to study how infection sensitizes lung to the damaging effects of total body irradiation (TBI) at infectious and TBI doses that individually do not cause injury. Mice infected with Pneumocystis carinii exhibited an asymptomatic, rapid, and transient influx of eosinophils and T cells in bronchoalveolar lavage fluid (BALF). In contrast, mice infected with P. carinii 7 days before receiving TBI and syngeneic BMT (P. carinii/TBI mice) exhibited severe pulmonary dysfunction, surfactant aggregate depletion, and surfactant activity reductions at 17 days post-BMT. BALF from P. carinii/TBI mice contained a disproportionate initial influx of CD4(+) T cells (CD4(+):CD8(+) ratio of 2.7) that correlated with progressive lung injury (from 8 to 17 days post-BMT). Levels of TNF-alpha in BALF were significantly increased in P. carinii/TBI mice compared with mice given either insult alone, with peak values found at 11 days post-BMT. In vivo depletion of CD4(+) T cells in P. carinii/TBI mice abrogated pulmonary dysfunction and reduced TNF-alpha levels in BALF, whereas depletion of CD8(+) T cells did not affect lung compliance or TNF-alpha. Lung injury was not attributable to direct P. carinii damage, since CD4-depleted P. carinii/TBI mice that exhibited no injury had higher average lung P. carinii burdens than either mice given P. carinii alone or undepleted P. carinii/TBI mice. Together, these results indicate that P. carinii infection can sensitize the lung to subsequent TBI-mediated lung injury via a process dependent on non-alloreactive CD4(+) T cells.

Animals↗
PubMed2005

Inhibition of surfactant activity by Pneumocystis carinii organisms and components in vitro.

This study examines the direct inhibitory effects of Pneumocystis carinii (Pc) organisms and chemical components on the surface activity and composition of whole calf lung surfactant (WLS) and calf lung surfactant extract (CLSE) in vitro. Incubation of WLS suspensions with intact Pc organisms (10(7) per milligram of surfactant phospholipid) did not significantly alter total phospholipid levels or surfactant protein A content. Incubation with intact Pc organisms also did not impair dynamic surface tension lowering in suspensions of WLS or centrifuged large surfactant aggregates on a bubble surfactometer (37 degrees C, 20 cycles/min, 0.5 and 2.5 mg phospholipid/ml). However, exposure of WLS or CLSE to disrupted (sonicated) Pc organisms led to severe detriments in activity, with minimum surface tensions of 17-19 mN/m vs. <1 mN/m for surfactants alone. Extracted hydrophobic chemical components from Pc (98.8% lipids, 0.1 mM) reduced the surface activity of WLS and CLSE similarly to sonicated Pc organisms, whereas extracted hydrophilic chemical components from Pc (primarily proteins) had only minor effects on surface tension lowering. These results indicate that in addition to surfactant dysfunction induced by inflammatory lung injury and edema-derived inhibitors in Pc pneumonia, disrupted Pc organisms in the alveolar lumen also have the potential to directly inhibit endogenous and exogenous lung surfactants in affected patients.

Animals↗
PubMed1998

Cell-specific expression of fibronectin and EIIIA and EIIIB splice variants after oxygen injury.

Cellular fibronectin (cFN) expression is characteristic of injured tissues. Unlike plasma FN, cFN mRNA often contains the EIIIA or EIIIB domains. We examined the lung cell-specific expression of total cFN mRNA and the EIIIA and EIIIB splice variants in rabbits after acute oxygen injury. By in situ hybridization, control lung had low cFN mRNA. After exposure to > 95% oxygen, mRNAs for total cFN and EIIIA were noted primarily in alveolar macrophages and large-vessel endothelial cells. By 3-5 days recovery, cFN and EIIIA mRNA abundance was increased in alveolar septal cells (i.e., alveolar epithelial, interstitial, or endothelial cells) and in some large-vessel endothelial cells but was low in bronchial epithelial cells. During recovery, EIIIB mRNA was low in alveolar septal cells but was noted mainly in chondrocytes. Immunostaining for EIIIA increased during recovery, paralleling the in situ hybridizations. Because FN may modulate alveolar type II cell phenotype, we investigated type II cell cFN mRNA expression in vivo. During recovery, neither isolated type II cells nor cells with surfactant protein C mRNA in vivo contained FN mRNA. In summary, these data suggest that cFN with the EIIIA domain has a role in alveolar cell recovery from oxygen injury and that type II cells do not express cFN during recovery.

Animals↗
PubMed2000

Mechanical strain-induced proliferation and signaling in pulmonary epithelial H441 cells.

Pulmonary epithelial cells are exposed to mechanical strain during physiological breathing and mechanical ventilation. Strain regulates pulmonary growth and development and is implicated in volutrauma-induced fibrosis. The mechanisms of strain-induced effects are not well understood. It was hypothesized that mechanical strain induces proliferation of pulmonary epithelial cells and that this is mediated by signals initiated within seconds of strain. To test this hypothesis, human pulmonary adenocarcinoma H441 cells were strained in vitro. Cyclic as well as tonic strain resulted in increased cellular proliferation. Western blot analysis of strained cells demonstrated three newly phosphorylated tyrosine residues within 30 s of strain. Phosphorylation of mitogen-activated protein kinases p42/44 increased, electrophoretic mobility shift assay demonstrated activation of transcription factor activating protein-1, and immunohistochemistry demonstrated increased phosphorylation of c-jun in response to strain. The tyrosine kinase inhibitor genistein blocked the strain-induced proliferation. We conclude that strain induces proliferation in pulmonary epithelial cells and that tyrosine kinase activity is necessary to signal the proliferative response to mechanical strain.

Cell Division↗
PubMed2005

Reactive oxidant and p42/44 MAP kinase signaling is necessary for mechanical strain-induced proliferation in pulmonary epithelial cells.

Mechanical strain is necessary for normal lung growth and development. Individuals with respiratory failure are supported with mechanical ventilation, leading to altered lung growth and injury. Understanding signaling pathways initiated by mechanical strain in lung epithelial cells will help guide development of strategies aimed at optimizing strain-induced lung growth while mitigating ventilator-induced lung injury. To study strain-induced proliferative signaling, focusing on the role of reactive oxidant species (ROS) and p42/44 mitogen-activated protein (MAP) kinase, human pulmonary epithelial H441 and MLE15 cells were exposed to equibiaxial cyclic mechanical strain. ROS were increased within 15 min of strain. N-acetylcysteine inactivated strain-induced ROS and inhibited p42/44 MAP kinase phosphorylation and strain-induced proliferation. PD98059 and UO126, p42/44 MAP kinase inhibitors, blocked strain-induced proliferation. To verify the specificity of p42/44 MAP kinase inhibition, cells were transfected with dominant-negative mitogen-activated protein kinase kinase-1 plasmid DNA. Transfected cells did not proliferate in response to mechanical strain. To determine whether strain-induced tyrosine kinase activity is necessary for strain-induced ROS-p42/44 MAP kinase signaling, genistein, a tyrosine kinase inhibitor, was used. Genistein did not block strain-induced ROS production or p42/44 MAP kinase phosphorylation. Gadolinium, a mechanosensitive calcium channel blocker, blocked strain-induced ROS production and p42/44 MAP kinase phosphorylation but not strain-induced tyrosine phosphorylation. These data support ROS production and p42/44 MAP kinase phosphorylation being involved in a common strain-induced signaling pathway, necessary for strain-induced proliferation in pulmonary epithelial cells, with a parallel strain-induced tyrosine kinase pathway.

Cell Line↗
PubMed2000

In vitro responses of gallbladder muscle from patients with acalculous biliary pain.

BACKGROUND: Diagnosis and identification of patients with acalculous biliary pain, who would benefit from surgery, remains a significant clinical problem. The cholecystokinin (CCK) provocation test helps diagnosis, but lack of consistency limits its usefulness. AIM: To characterize the response of gallbladder muscle strips, from patients with acalculous biliary pain, to hormonal and muscarinic stimulation and to compare these with strips from gallstone patients and normal controls. PATIENTS: Eleven patients with acalculous biliary pain were studied, 5 had a positive CCK test. Eight gallbladders from gallstone patients and 6 from partial hepatectomies were used for comparison. METHODS: Muscle strips from the body and neck of the gallbladder were suspended in organ baths and dose-response curves were constructed for CCK-8 and carbachol. RESULTS: In the acalculous group the strips from the body were less sensitive to carbachol than those of the neck. CONCLUSION: Since we found no differences in the CCK responses for the groups, it casts doubt over the effectiveness of the CCK test to diagnose acalculous biliary pain. Since carbachol sensitivity was different, it might be that a similar test using muscarinic stimulation would help in the diagnosis of this difficult group of patients.

Adult↗
PubMed1998

Latest developments in the field of neurotransmitters.

Receptors involved in neurotransmission are an important target for drug therapy and the identification and development of receptor-specific compounds is an essential part of contemporary drug development. Antagonists acting at detrusor muscarinic receptors and prostatic adrenergic receptors are now established therapies for the treatment of bladder instability and benign prostatic hyperplasia, respectively. Future developments await the results of basic pathophysiological studies to establish the role of classical and nonadrenergic, noncholinergic neurotransmission in the development and maintenance of diseases of the lower urinary tract. With the development of better pharmacological tools and molecular biological techniques, receptor properties are likely to be found to be tissue-specific, making the development of drugs with true tissue specificity and fewer side effects a reality.

Female↗