Biomedical subjects

R W Alexander

Publications and source records attributed to R W Alexander.

At least 55 records · Page 3Linked to original sources

PubMed1997

Risk factors for methotrexate-induced lung injury in patients with rheumatoid arthritis. A multicenter, case-control study. Methotrexate-Lung Study Group.

BACKGROUND: Toxicity limits the use of methotrexate. OBJECTIVE: To identify risk factors for methotrexate-induced lung injury in patients with rheumatoid arthritis. DESIGN: Case-control study. SETTING: One private and five academic rheumatology practices. PARTICIPANTS: Methotrexate recipients with rheumatoid arthritis with and without lung injury. MEASUREMENTS: Potential risk factors examined were sociodemographic and lifestyle characteristics, medical history, clinical and ancillary features and treatment of rheumatoid arthritis before methotrexate therapy, and characteristics of methotrexate therapy. Cases of lung injury were defined according to the modified criteria of Searles and McKendry. RESULTS: Ninety-four percent of the study participants were white, and 67% were women. Case-patients (n = 29) were older than controls (n = 82) (61.5 compared with 54.5 years of age). The strongest predictors of lung injury, after adjustment for other variables, were older age (odds ratio [OR], 5.1 [95% CI, 1.2 to 21.1]), diabetes (OR, 35.6 [CI, 1.3 to infinity]), rheumatoid pleuropulmonary involvement (OR, 7.1 [CI, 1.1 to 45.4]), previous use of disease-modifying antirheumatic drugs (OR, 5.6 [CI, 1.2 to 27.0]), and hypoalbuminemia (OR, 19.5 [CI, 3.5 to 109.7]). Previous use of disease-modifying antirheumatic drugs and hypoalbuminemia had very large attributable risks. CONCLUSION: Knowledge of the risk factors that predispose patients with rheumatoid arthritis to the toxic effects of methotrexate on the lung may provide a rationale for monitoring high-risk patients and may facilitate their management.

Antirheumatic Agents↗

PubMed1997

Perceived physical and emotional trauma as precipitating events in fibromyalgia. Associations with health care seeking and disability status but not pain severity.

OBJECTIVE: We examined relationships between perceived physical and emotional trauma that occur prior to, or that initiate, pain onset and health care seeking for fibromyalgia syndrome (FMS). We also assessed associations between perceived trauma and levels of health care usage, symptom severity, functional disability, and receipt of disability compensation among patients with FMS. METHODS: We evaluated these variables using interviews and standardized instruments in a consecutive series of FMS patients and community residents who met the American College of Rheumatology criteria for FMS but had not sought medical care ("nonpatients"). RESULTS: Emotional trauma was associated with status as an FMS patient independently of demographics, physical trauma, and sexual/physical abuse (P = 0.007). Among patients, emotional trauma was related to a high number of physician visits (P = 0.013), functional disability ratings (P = 0.012), and fatigue (P = 0.029), but physical trauma was associated with receipt of disability compensation (P = 0.019). Trauma history was not related to pain severity or pain thresholds. CONCLUSION: Perception of physical trauma is a greater determinant of disability compensation for FMS than is perceived emotional trauma, symptom severity, or functional disability. Effort should be devoted to understanding the social and legal factors underlying this observation, as well as to reducing high health care usage among FMS patients with emotional trauma.

Adolescent↗

PubMed1997

Clinical, laboratory, radiographic, and histopathologic features of methotrexate-associated lung injury in patients with rheumatoid arthritis: a multicenter study with literature review.

OBJECTIVE: To describe the clinical, laboratory, radiologic, and histopathologic features of methotrexate (MTX)-induced lung injury in a combined cohort of selected patients with rheumatoid arthritis (RA) and all cases reported in the English-language literature. METHODS: Retrospective combined cohort review and abstraction from the medical literature. Case reports were obtained from 6 centers that had 4 or more cases of potential MTX lung injury per site. RA patients who were seen between 1981 and 1993 and who satisfied predetermined criteria for the presence of MTX lung injury were identified. RESULTS: Twenty-seven patients satisfied the criteria for definite MTX lung injury, and 2 for probable MTX lung injury. Predominant clinical features of MTX lung injury included shortness of breath in 27 patients (93.1%), which was present for 23.5 +/- 22.3 days (mean +/- SD), cough in 24 (82.8%), present for 26.9 +/- 28.5 days, and fever in 20 (69.0%), present for 10.4 +/- 12.8 days. Five patients (17.2%) died, compared with 12 of 68 (17.6%) reported in the medical literature. Four of the 6 patients who were re-treated with MTX after an initial pulmonary event developed recurrent lung toxicity, resulting in 2 deaths, compared with a recurrence rate of 3 of 6 in the literature. CONCLUSION: MTX lung injury is most often a subacute process, in which symptoms are commonly present for several weeks before diagnosis. Approximately 50% of the cases are diagnosed within 32 weeks from initiation of MTX treatment. A patient who recovers from MTX lung injury should not be re-treated. Earlier recognition and drug withdrawal may avoid the serious and sometimes fatal outcome that has been observed in this and other studies.

Aged↗

PubMed1997

Cyclic strain induces an oxidative stress in endothelial cells.

Hypertension imposes an oxidant stress on the aorta and also causes mechanical deformation of the aortic wall. To assess whether deformation causes an oxidative stress, isolated porcine aortic endothelial cells (PAEC) were subjected to cyclic strain, and the cumulative amount of thiobarbituric acid reactive substances (TBARS, an index of lipid peroxidation) and H2O2 (a reactive oxygen species) was measured in the eluent at 2, 6, and 24 h. TBARS were increased by 40.5 +/- 9.2% after 24 h in cells exposed to cyclic strain vs. static controls (P < 0.05). No difference was seen at 2 and 6 h. H2O2 release was increased after 6 and 24 h of cyclic strain by 22.0 +/- 8.0 and 57.6 +/- 11.1 nmol H2O2/mg, respectively (P < 0.005), but was not increased after 2 h of strain. In vascular smooth muscle cells, TBARS were not observed and H2O2 release was not increased by cyclic strain. To investigate a potential source of H2O2 induced by strain, the activity of NADH/NADPH oxidase, a superoxide-generating enzyme, was measured by chemiluminescence. After 2 h, cells exposed to cyclic strain had greater activity than static controls (531.0 +/- 68.4 vs. 448.3 +/- 54.2 pmol O2- x mg(-1) x s(-1), respectively, when incubated with NADH, P < 0.005; 85.8 +/- 8.9 vs. 71.6 +/- 3.8 pmol O2- x mg(-1) x s(-1) when incubated with NADPH, P < 0.05). No effect on NADH/NADPH oxidase activity was seen after 6 or 24 h. The following conclusions were made: 1) cyclic strain induces an oxidant stress in PAEC monolayers as measured by TBARS formation and H2O2 release, 2) NADH/NADPH oxidase is a potential source of H2O2 release in cyclically strained cells, and 3) mechanical deformation of endothelial cells may play a critical role in the generation of oxidative stress within the vessel wall.

Animals↗

PubMed1997

Angiotensin II signaling in vascular smooth muscle. New concepts.

Angiotensin II is a multifunctional hormone that affects both contraction and growth of vascular smooth muscle cells through a complex series of intracellular signaling events initiated by the interaction of angiotensin II with the AT1 receptor. The cellular response to angiotensin II is multiphasic, involving stimulation within seconds of phospholipase C and Ca2+ mobilization; activation within minutes of phospholipase D, A2, protein kinase C, and MAP kinase; and stimulation after a period of hours of gene transcription and NADH/NADPH oxidase activity. Angiotensin II also activates numerous intracellular tyrosine kinases. In this respect, it shares some aspects of signaling with growth factor and cytokine receptors, including activation of phospholipase C-gamma, src, and ras; association of shc with grb2; and stimulation of the Jak/STAT pathway. The cellular events responsible for this unique series of events may involve receptor movement and the creation of a signaling domain. Elucidation of these pathways is important to our understanding of AT1 receptor function as a final effector of the renin-angiotensin system.

Angiotensin II↗

PubMed1997

Monocyte chemoattractant protein-1 expression in aortic tissues of hypertensive rats.

Monocyte chemoattractant protein-1 (MCP-1), a potent monocyte chemoattractant synthesized by vascular cells and monocytes, has been proposed to be an important mediator of inflammatory responses in the arterial vasculature. It was recently demonstrated that hypertension is associated with an inflammatory response in the arterial wall. To determine the effect of hypertension on arterial MCP-1 expression, we induced hypertension in Sprague-Dawley rats by infusing angiotensin II (0.75 mg x kg[-1] x d[-1] SC) for 7 days. Using Northern blot analysis, we detected a 3.6-fold increase in MCP-1 mRNA in the aortas of hypertensive rats. When we normalized blood pressure in angiotensin II-treated rats through oral administration of the nonspecific vasodilator hydralazine (15 mg x kg[-1] x d[-1]), aortic MCP-1 mRNA expression was significantly reduced. Similar results were obtained with a norepinephrine model of hypertension. Taken together, these data suggest that mechanical factors may be responsible in part for the upregulation of expression. Consistent with this interpretation, we found that cultured rat aortic vascular smooth muscle cells exposed to mechanical strain (20% peak deformation at 1 Hz) exhibited a marked increase in MCP-1 expression, suggesting the hemodynamic strain imparted onto arterial cells in hypertension is an important stimulus underlying this phenomenon. These results provide important insights into the in vivo regulation of MCP-1 and have potential implications for understanding the influence of hypertension on atherosclerosis.

Angiotensin II↗

PubMed1997

Vascular thrombin receptor regulation in hypertensive rats.

Thrombin has been implicated as an important mediator of vascular lesion formation in atherosclerosis and restenosis. To investigate a potential role for thrombin signaling in the vascular response to hypertension, we have studied thrombin receptor (TR) expression and regulation in hypertensive rats. Aortic TR mRNA was upregulated by angiotensin II (Ang II)-induced hypertension (10.7 +/- 2.5 times control, P < .02), which correlated with a 4-fold increase in thrombin-induced constriction in isolated endothelium-denuded aortic rings. The AT1 receptor antagonist losartan normalized blood pressure and TR mRNA. Conversely, lowering blood pressure to the same degree with hydralazine did not abolish the upregulation of TR mRNA expression. When low-renin low-Ang II hypertension was induced in Dahl salt-sensitive rats, there was no detectable increase in the expression of aortic thrombin receptor mRNA. Finally, treatment with a chimeric heparin-binding form of the recombinant human Cu/Zn superoxide dismutase caused complete inhibition of TR mRNA upregulation, suggesting that an increased rate of superoxide anion production is an important signaling mechanism. Thus, increased TR expression via a redox-sensitive mechanism in the aortic smooth muscle of rats treated with Ang II represents a novel in vivo mechanism through which the hypertensive effects of Ang II are mediated.

Angiotensin II↗

PubMed1996

Exacerbation of atherosclerosis by hypertension. Potential mechanisms and clinical implications.

Recent experimental data suggest marked similarities between the effects of hypertension and hypercholesterolemia on the arterial intima. Both conditions also seem to exert proinflammatory effects on the artery, resulting in the recruitment of monocytes into the intima. These effects may be due to production of oxygen-free radicals, which in turn may stimulate genes involved in the recruitment of inflammatory cells into the arterial wall. Plaque rupture and acute myocardial infarction are related to local accumulation of inflammatory cells in vulnerable areas of the plaque. Recent clinical trials using cholesterol-lowering or antihypertensive therapies have shown a decrease in cardiovascular events that may have resulted from withdrawal of inflammatory effects on the arterial wall. Angiotensin-converting enzyme inhibitors decrease the rate of myocardial infarction in patients with overt congestive heart failure or left ventricular dysfunction. These drugs probably affect several mechanisms related to the inhibition of angiotensin production and the potentiation of bradykinin and resultant enhancement of nitric oxide and prostacyclin. The mechanisms could include reversing the proinflammatory effects of angiotensin and hypercholesterolemia on the arterial wall. Future therapeutic strategies of vascular protection in hypertension may include direct attacks on proinflammatory or pro-oxidant vascular mechanisms.

Animals↗

PubMed1996

Nitric oxide regulates vascular cell adhesion molecule 1 gene expression and redox-sensitive transcriptional events in human vascular endothelial cells.

Decreased nitric oxide (NO) activity, the formation of reactive oxygen species, and increased endothelial expression of the redox-sensitive vascular cell adhesion molecule 1 (VCAM-1) gene in the vessel wall are early and characteristic features of atherosclerosis. To explore whether these phenomena are functionally interrelated, we tested the hypothesis that redox-sensitive VCAM-1 gene expression is regulated by a NO-sensitive mechanism. In early passaged human umbilical vein endothelial cells and human dermal microvascular endothelial cells, the NO donor diethylamine-NO (DETA-NO, 100 microM) reduced VCAM-1 gene expression induced by the cytokine tumor necrosis factor alpha (TNF-alpha, 100 units/ml) at the cell surface level by 65% and intracellular adhesion molecule 1 (ICAM-1) gene expression by 35%. E-selectin gene expression was not affected. No effect on expression of cell adhesion molecules was observed with DETA alone. Moreover, DETA-NO suppressed TNF-alpha-induced mRNA accumulation of VCAM-1 and TNF-alpha-mediated transcriptional activation of the human VCAM-1 promoter. Conversely, treatment with NG-monomethyl-L-arginine (L-NMMA, 1 mM), an inhibitor of NO synthesis, augmented cytokine induction of VCAM-1 and ICAM-1 mRNA accumulation. By gel mobility shift analysis, DETA-NO inhibited TNF-alpha activation of DNA binding protein activity to the VCAM-1 NF-kappa B like binding sites. Peroxy-fatty acids such as 13-hydroperoxydodecanoeic acid (linoleyl hydroperoxide) may serve as an intracellular signal for NF-kappa B activation. Using thin layer chromatography, DETA-NO (100 microM) suppressed formation of this metabolite, suggesting that DETA-NO modifies the reactivity of oxygen intermediates in the vascular endothelium. Through this mechanism, NO may function as an immunomodulator of the vessel wall and thus mediate inflammatory events involved in the pathogenesis of atherosclerosis.

Antioxidants↗

PubMed1996

Phosphorylation of the type 1A angiotensin II receptor by G protein-coupled receptor kinases and protein kinase C.

The type 1A angiotensin II receptor (AT1A-R), which mediates cardiovascular effects of angiotensin II, has been shown to undergo rapid agonist-induced desensitization. We investigated the potential role of second messenger-activated kinases and G protein-coupled receptor kinases (GRKs) in the regulation of this receptor. In 293 cells transfected with the AT1A-R, a 3-min challenge with angiotensin II engendered a 46% decrease in subsequent angiotensin II-stimulated phosphoinositide hydrolysis in intact cells. This agonist-induced desensitization correlated temporally and dose-dependently with the phosphorylation of the receptor to a stoichiometry of 1 mol of phosphate/mol of receptor, as assessed by immunoprecipitation of receptors from cells metabolically labeled with 32Pi. Agonist-induced receptor phosphorylation was reduced by 40-50% by either overexpression of a dominant negative K220R mutant GRK2 or treatment of the cells with the protein kinase C (PKC) inhibitor staurosporine, in a virtually additive fashion. Cellular overexpression of GRK2K220R not only inhibited agonist-induced AT1A-R phosphorylation, but also prevented receptor desensitization, as assessed by angiotensin II-stimulated GTPase activity in membranes prepared from agonist-treated and control cells. In contrast, PKC inhibition by staurosporine did not affect homologous desensitization of the AT1A-R. Overexpression of GRKs 2, 3, or 5 significantly augmented the agonist-induced AT1A-R phosphorylation 1.5- to 1.7-fold (p < 0.001). These findings suggest a role for receptor phosphorylation by one or several GRKs in the rapid agonist-induced desensitization of the AT1A-R.

Amino Acid Sequence↗

PubMed1996

Psychiatric diagnoses in patients with fibromyalgia are related to health care-seeking behavior rather than to illness.

OBJECTIVE: To compare the frequency of lifetime psychiatric disorders among 3 groups of subjects: patients with fibromyalgia syndrome (FMS) from a tertiary care setting, community residents with FMS who had not sought medical care for their FMS symptoms ("FMS nonpatients"), and healthy controls. METHODS: We used the Computerized Diagnostic Interview Schedule to assess lifetime psychiatric diagnoses, as well as the Center for Epidemiological Studies Depression scale and the Trait Anxiety Inventory to assess current psychological distress, among 64 patients with FMS, 28 FMS nonpatients, and 23 healthy individuals. RESULTS: Patients with FMS, relative to FMS nonpatients and healthy controls, were characterized by a significantly greater number of lifetime psychiatric diagnoses (P = 0.002). Nonpatients did not differ from controls in psychiatric diagnoses. Patients also exhibited higher psychological distress levels than nonpatients, and nonpatients showed greater distress than controls. Differences in psychological distress between patients and nonpatients were eliminated after controlling for pain threshold and fatigue ratings. CONCLUSION: Psychiatric disorders are not intrinsically related to the FMS syndrome. Instead, multiple lifetime psychiatric diagnoses may contribute to the decision to seek medical care for FMS in tertiary care settings.

Adolescent↗

PubMed1996

Asthma and gastroesophageal reflux: acid suppressive therapy improves asthma outcome.

PURPOSE: To determine (1) the appropriate omeprazole (Prilosec) dose required for adequate acid suppression in asthmatics with gastroesophageal reflux, (2) whether aggressive acid suppressive therapy of gastroesophageal reflux improves asthma outcome in asthmatics with gastroesophageal reflux, (3) the time course of asthma improvement, and (4) demographic, esophageal, or pulmonary predictors of a positive asthma response to antireflux therapy. PATIENTS AND METHODS: Thirty nonsmoking adult asthmatics with gastroesophageal reflux (asthma defined by American Thoracic Society criteria and reflux defined by symptoms and abnormal 24-hour esophageal pH testing) were recruited from the outpatient clinics of a 900-bed university hospital. Patients underwent baseline studies including a demographic questionnaire, esophageal manometry, dual-probe 24-hour esophageal pH test, barium esophogram, and pulmonary spirometry. During the 4-week pretherapy phase, patients recorded reflux and asthma symptom scores and peak expiratory flow rates (PEFs) upon awakening, 1 hour after dinner, and at bedtime. Patients began 20 mg/d omeprazole, and the dose was titrated until acid suppression was documented by 24-hour pH test. Patients remained on this acid suppressive dose for 3 months. Responders were identified by a priori definitions: asthma symptom reduction by >20% and/or PEF increase by >20%. Asthma symptom scores, PEF's baseline and posttherapy pulmonary spirometry were analyzed. RESULTS: Twenty-two (73%) patients were asthma symptom and /or PEF responders: 20 (67%) were asthma symptom responders, and 6 (20%) were PEF responders. Responders reduced their asthma symptoms by 57% (P<0.001), improved their morning and night PEFs by 8% and 9% (both P <0.005), and had improvement in forced expiratory volume at 1 second (P <0.02), mean forced expiratory flow during the middle half (25% to 75%) of the forced vital capacity (P <0.04), and peak expiratory flow (P <0.01) with acid suppressive therapy. Mean acid suppressive dose of omeprazole was 27 mg/d (+/-2.2) with 27% (8) patients requiring more than 20 mg/d. The presence of regurgitation or excessive proximal esophageal reflux predicted asthma response with 100% sensitivity, 100% negative predictive value, specificity of 44% and a positive predictive value of 79%. CONCLUSIONS: Acid suppressive therapy with omeprazole improves asthma symptoms and/or PEFs by >20% and improves pulmonary function in 73% of asthmatics with gastroesophageal reflux after 3 months of acid suppressive therapy. Many asthmatics (27%) required >20 mg/d of omeprazole to suppress acid. The presence of regurgitation and/or excessive proximal esophageal reflux predicts a positive asthma outcome.

Adult↗

PubMed1996

Endothelial control of the cardiovascular system: recent advances.

The endothelium is uniquely positioned at the interface between the blood and the vessel wall. As such, it performs multiple functions: It is involved in the regulation of coagulation, leukocyte adhesion in inflammation, vessel tone, and vascular smooth muscle cell growth, and also acts as a barrier to transvascular flux of liquids and solutes. Far from being a passive participant in these events, it is a dynamic tissue, secreting and modifying vasoactive substances, influencing the behavior of other cell types, and regulating extracellular matrix production and composition. During the past 20 years, the endothelium has been the focus of intense experimental work, resulting in the evolution of a new appreciation of its potential role in vascular disease. This review will concentrate on several areas of endothelial biology in which our knowledge of the molecular mechanisms regulating the function of the endothelium has expanded considerably, permitting new insights into the pathogenesis of vascular disease.

Animals↗

PubMed1996

Angiotensin receptors and their therapeutic implications.

Angiotensin II is a multifunctional hormone that exerts its effects by interacting will cell surface receptors. Two major subtypes of receptors (AT1 and AT2) have been distinguished by pharmacological and molecular biological techniques. AT1 receptors have been further subdivided into AT1A and AT1B receptors. Several other isoforms have been found, notably in nonmammalian systems, but further information is necessary before definitive classification can be made. AT1 receptors mediate most known functions of angiotensin II, while AT2 receptors may be important developmentally. The molecular, structural, and biochemical characteristics of these receptors have been described, as well as the factors that regulate their expression. This receptor system has been implicated in several cardiovascular diseases, including hypertension, restenosis after angioplasty, cardiac hypertrophy, heart failure, myocardial infarction, and ventricular remodeling. Structural analysis of AT receptors may provide the basis for the development of new therapeutic agents with enhanced specificity for the treatment of these diseases.

Amino Acid Sequence↗

PubMed1996

Signal transduction in vascular smooth muscle.

INTRODUCTION: Vascular smooth muscle participates in the normal control of vascular tone and in the pathological adaptation of arteries in hypertension and atherosclerosis. Growth factors and vasoconstrictors activate overlapping signalling pathways that include activation of phospholipase C isoforms, phospholipase D, protein kinase C, tyrosine kinases and mitogen-activated protein kinases. ANGIOTENSIN II AS A PARADIGM OF A MULTIFUNCTIONAL HORMONE: Angiotensin II initiates a biphasic sequence of second messenger generation in vascular smooth muscle cells that appears to result from signalling that occurs in two distinct domains involving aggregated and sequestered receptors. It also activates membrane-associated reduced nicotinamide adenine dinucleotide/reduced nicotinamide adenine dinucleotide phosphate oxidases that contribute to the control of the redox state of the cell. CONCLUSION: Vasoactive agents generate a complex signalling pattern that controls both the normal and pathophysiological responses of vascular smooth muscle.

Angiotensin II↗

PubMed1995

Cytochrome b-558 alpha-subunit cloning and expression in rat aortic smooth muscle cells.

Recent studies have shown that the NADPH oxidase participates in the generation of superoxide anion in non-phagocytic cells. Here we report the isolation and nucleotide sequence of a cDNA for the cytochrome b-558 alpha-subunit of the NADPH oxidase in rat vascular smooth muscle cells (VSMCs). The coding region of the cDNA was 93% homologous to mouse and 81% to human in nucleotide sequence and 96% homologous to mouse and 89% to human in the deduced amino acid sequence. Our results provide a tool with which to explore the mechanism of superoxide anion generation in rat VSMCs and other non-phagocytic cells.

Amino Acid Sequence↗

PubMed1995

Cell type-specific transactivation of the VCAM-1 promoter through an NF-kappa B enhancer motif.

Cytokine activation of vascular cell adhesion molecule-1 (VCAM-1) gene expression by endothelial cells is an important feature in a variety of vascular inflammatory responses. Cytokines transcriptionally activate the VCAM-1 promoter in endothelial cells at least in part through two closely linked NF-kappa B enhancer motifs, kappa L-kappa R (positions -77 and -63). However, cytokine activation of the dimeric NF-kappa B transcriptional factor (p50+p65 subunits) occurs in almost all cell types, whereas VCAM-1 gene expression exhibits a cell type-specific pattern of expression. Tumor necrosis factor-alpha markedly transactivated a transiently transfected minimal kappa L-kappa R motif-driven VCAM-1 promoter, p85VCAMCAT, in passaged human vascular endothelial cells but not in the human epithelial cell line, HeLa suggesting that cell type-specific factors may function through the kappa L-kappa R motif. Both cell types exhibited similar inductions of NF-kappa DNA binding activity and transcriptional activity. However, co-transfection of HeLa cells with p65 and p50 expression vectors demonstrated that the minimal VCAM-1 promoter was effectively transactivated by p65 alone but that additional co-expression of p50 blocked this activity. Furthermore, cytokine activation of the minimal VCAM-1 promoter in HeLa cells was recovered by inhibition of p50 expression using antisense oligonucleotide. These studies suggest that the NF-kappa B(p50+p65 heterodimer) does not support transactivation of the VCAM-1 promoter with the p50 subunit potentially playing a significant inhibitory role in suppressing cytokine activation of VCAM-1. In addition, p65 associated transcriptional factors other than NF-kappa B may serve as positive, cytokine-inducible, cell type-specific regulators of VCAM-1 gene expression.

Base Sequence↗

PubMed1995

The vessel wall.

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Animals↗