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At least 685 records · Page 38Linked to original sources
PubMed1998

RANTES activation of phospholipase D in Jurkat T cells: requirement of GTP-binding proteins ARF and RhoA.

The chemokine RANTES is a potent agonist of T cell activation. In an investigation of signal-transduction events activated by this chemokine, we have shown that RANTES stimulates dose-dependent phospholipase D (PLD) activity in Jurkat cells. Equilibrium-binding analyses using 125I-labeled RANTES indicated the presence of a receptor for RANTES on these cells, which has a Kd of 0.1 nM, is expressed at approximately 600 sites per cell, and a binding specificity that was not comparable with that of any of the known chemokine receptors, since 125I-labeled RANTES was displaced by macrophage-inflammatory protein-1 beta (but not macrophage-inflammatory protein-1 alpha), monocyte-chemotactic protein-1 (MCP-1), MCP-3, MCP-4, and eotaxin. RANTES-induced PLD activation was augmented by GTP gamma S, but not GDP beta S, and inhibited by the protein kinase C inhibitor bisindolylmaleimide, as well as the fungal metabolite brefeldin A, and C3 exoenzyme (Clostridium botulinum), implicating the activation of RhoA. RANTES also induced GTP-GDP exchange of immunoprecipitated RhoA. RANTES-stimulated PLD activity was dependent on an ADP-ribosylation factor(s), as assessed by inhibition studies using a synthetic inhibitory peptide of the N-terminal 16 amino acids of ADP-ribosylation factor 1. These studies indicate the potential existence of a novel receptor-mediated mechanism for activation of T cells by the chemokine RANTES.

ADP-Ribosylation Factors↗
PubMed2000

Epidemiology of de novo acute renal failure in hospitalized African Americans: comparing community-acquired vs hospital-acquired disease.

BACKGROUND: The high incidence and prevalence of end-stage kidney disease among African Americans is well known, but the epidemiology of acute renal failure (ARF) among African Americans is unknown. This study was designed to determine the incidence, associated risk factors, and prognosis of ARF in hospitalized African Americans and to compare these variables in hospital-acquired ARF (HA-ARF) against community-acquired ARF (CA-ARF). METHODS: A 3-year (1994-1996), computer-assisted retrospective analysis of hospital discharges with confirmed diagnoses of ARF. One hundred of 240 cases met the inclusion criteria for de novo ARF. Demographic, laboratory, and clinical profiles of all patients were retrieved and subdivided into CA-ARF and HA-ARF. Both analysis of variance and chi2 tests were used for analysis. Survival regression used both the Cox proportional hazards and Kaplan-Meier models. RESULTS: The incidence of CA-ARF was 3.5 times greater than that of HA-ARF (0.55% vs 0.15%). The mean age of all patients was 54 years with a 67% male predominance. There were no significant differences in age, sex, peak serum creatinine levels, or underlying medical history. Prerenal causes of ARF were more common among CA-ARF than HA-ARF (35% vs 19%; P = .07), but intra-renal causes were more common among HA-ARF (81% vs 55%; P = .07). All cases of obstruction occurred in CA-ARF. Mortality was higher in HA-ARF (59% vs 33%; P = .03), and the incidence of recognized predictors of mortality was higher in patients with HA-ARF than in those with CA-ARF: oliguria (59% vs 35%; P = .04); sepsis (73% vs 35%; P = .004); stay in the intensive care unit (ICU) or mechanical ventilation (55% vs 6%; P<.001); and multiorgan failure (59% vs 24%; P = .002). Those with HA-ARF were twice as likely to require dialysis as those with CA-ARF. The mortality was high in younger patients with CA-ARF and in older patients with HA-ARF, but the dialysis-related mortality rate was 3-fold higher among patients with HA-ARF. While mean +/- SD length of hospital stay was more prolonged in HA-ARF than CA-ARF (26 +/- 28 days vs 12 +/- 11 days; P<.001), the 120-day survival rate was lower in HA-ARF than CA-ARF (43% vs 66%; P = .05). The HA-ARF status was associated with a relative risk of 2.5 (confidence interval, 1.1-5.5; P = .03) for shortened survival. CONCLUSIONS: The overall epidemiologic characteristics of ARF among hospitalized African Americans seem to be comparable to those in whites, but the difference in incidence between CA-ARF and HA-ARF was much higher in African Americans. In view of the high mortality and morbidity rates associated with ARF and the fact that younger African American patients with CA-ARF were more likely to die than their older counterparts, we recommend that renal failure awareness be incorporated into community-based health educational programs in African American populations.

Acute Kidney Injury↗
PubMed2005

[Comparison of clinical characteristics between hospital-acquired and community-acquired acute renal failure].

OBJECTIVE: To investigate the differences between hospital-acquired acute renal failure (HA-ARF) and community-acquired acute renal failure (CA-ARF) in epidemiology, etiology and prognosis. METHODS: The diagnosis of ARF of patients diagnosed with ARF from ICD-9 codes, who were discharged from Peking University Third Hospital from January 1994 to December 2003, was reconfirmed and categorized by two nephrologists independently. The indexes of epidemiology, etiology and prognosis were studied. Single-variable analysis and multivariate logistic regression analysis were performed to investigate the correlation between clinical features and prognosis respectively. RESULTS: Two hundred and five cases were collected and all were reconfirmed. CA-ARF had a predominance of 59.5%. HA-ARF, however, increased by 1.06 times in last 5 years (P<0.05); 59.0% of HA-ARF was diagnosed in department of surgery while 70.5% of CA-ARF was in medical department (both P<0.05); 36.1% HA-ARF patients had two or more pathogenic causes, while 91.2% CA-ARF only had one cause (P<0.05); 49.4% HA-ARF developed after operation; 26.5% HA-ARF and 18.8% CA-ARF were drug-related (P>0.05); 24.1% HA-ARF and 12.3% CA-ARF were infection-related (P=0.028). Mortality and recovery rates were 62.7% and 20.6%, respectively, in HA-ARF while 23.0% and 67.2% in CA-ARF respectively (both P<0.01). The percentage of oliguria, multiple organ failure (MOF), systemic inflammatory response syndrome (SIRS), and use of mechanical ventilation were significantly higher in HA-ARF than in CA-ARF (all P<0.01). Acute tubule necrosis-injury severity score (ATN-ISS), acute pathological and chronic health evaluation (APACHE II) score were 0.54+/-0.24 and 19.6+/-4.9 in HA-ARF, while they were 0.27+/-0.18 and 15.7+/-5.6 in CA-ARF (both P<0.01). Multiple regression analysis identified that both MOF and SIRS were common independent risk factors for HA-ARF and CA-ARF, and oliguria and advanced age were respective independent risk factor for HA-ARF and CA-ARF. CONCLUSION: CA-ARF prevails in hospitalized Chinese patients during the last 10 years, but HA-ARF is increasing in incidence significantly during the last 5 years. The etiology is mostly simple and the prognosis is relatively good in CA-ARF, while the pathogenic cause is mostly complicated and the outcome is much poorer in HA-ARF.

Acute Kidney Injury↗
PubMed1987

Platelet function in acute respiratory failure.

To assess the role of platelets in thrombohemorrhagic complications of acute respiratory failure (ARF), we studied platelet function in 13 ARF patients admitted for intensive care, in six acutely ill intensive care patients without evidence of acute lung injury (non-ARF), and in 10 normal subjects. Platelet counts in ARF and non-ARF patients were similar to the normal range. The bleeding time of the ARF patients (8.5 +/- 0.9 min) was significantly longer (p less than 0.01) than the normal (4.8 +/- 0.2 min) but similar to non-ARF patients (5.4 +/- 0.8 min). The bleeding time prolongations in ARF patients were unrelated to platelet concentration. Platelet aggregation induced by ADP and thrombin was normal in both ARF and non-ARF patient groups. The epinephrine response was impaired in one non-ARF patient and in three ARF patients; collagen-induced aggregation was absent in two ARF patients, with a prolonged bleeding time. Levels of VIII:C and vWF in both groups of patients were similar to the normal level, but VIIIR:Ag levels in ARF patients (407 +/- 45% of normal) were higher (p less than 0.01) than in both non-ARF patients (210% +/- 10%) and normal subjects (106% +/- 4). The electrophoretic mobility of VIIIR:Ag was abnormal in ARF patients. The prolonged bleeding time in ARF patients appears to result from the qualitative and quantitative VIIIR:Ag defect. beta-Thromboglobulin levels were greater (p less than 0.01) in ARF patients (87.6 +/- 6.9 ng/ml; p less than 0.001) than in non-ARF patients (46.2 +/- 3.1 ng/ml) or in normal subjects (25.3 +/- 2.5 ng/ml p less than 0.0001). However, platelet factor 4 plasma levels in ARF patients (18 +/- 1.6 ng/ml) did not differ from those in non-ARF patients (15.0 +/- 3.0 ng/ml), but both were significantly different from normal (6.1 +/- 0.8 ng/ml). Plasma thromboxane B2 (T X B2) levels were not different from normal values in either ARF or non-ARF patients, but 6-keto-PGF1 alpha levels were significantly reduced (p less than 0.01) in ARF patients (215 +/- 43 pg/ml) compared to normal values (381 +/- 34 pg/ml). Non-ARF patients had 6-keto-PGF1 alpha levels (285 +/- 111 pg/ml) midway between the normal values and those of ARF patients. Our results suggest that in vivo platelet activation occurs in ARF. ARF patients have quantitative and qualitative platelet defects that may contribute to thrombotic and hemorrhagic complications.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Molecular identification of ADP-ribosylation factor mRNAs and their expression in mammalian cells.

ADP-ribosylation factors (ARFs) are approximately 20-kDa guanine nucleotide-binding proteins that serve as GTP-dependent allosteric activators of cholera toxin ADP-ribosyltransferase activity. Four species of mammalian ARF, termed ARF 1-4, have been identified by cloning. Hybridization of a bovine ARF 2 cDNA under low stringency with mammalian poly(A)+ RNA resulted in multiple bands that were subsequently assigned to the known ARF genes using ARF-specific oligonucleotide probes. The relative signal intensities of some bands (e.g. the 3.8- and 1.3-kilobase (kb) mRNAs) that hybridized with the cDNA were not, however, consistent with the intensities observed with the individual ARF-specific oligonucleotide probes. These inconsistencies suggested that other ARF-like mRNAs were comigrating with known ARF mRNAs. To explore this possibility, a cyclic AMP-differentiated HL-60 Lambda ZAP library was screened using the bovine ARF 2 cDNA. Clones corresponding to known ARF genes (1, 3, and 4) were identified by hybridization of positive clones with oligonucleotide probes specific for each ARF species; ARF 2 cDNA-positive, oligonucleotide-negative clones were sequenced. Two new ARF-like genes, ARF 5 and 6, encoding proteins of 180 and 175 amino acids, respectively, were identified. Both proteins contain consensus sequences believed to be involved in guanine nucleotide binding and GTP hydrolysis. ARF 5 was most similar in deduced amino acid sequence to ARF 4, which also has 180 amino acids. ARF 6, whose deduced amino acid sequence is identical with that of a putative chicken pseudogene (CPS1) except for a serine/threonine substitution, was different from other ARF species in size and deduced amino acid sequence. With mammalian poly(A)+ RNA from a variety of tissues and cultured cells, ARF 5 preferentially hybridized with a 1.3-kb mRNA, whereas ARF 6 hybridized with 1.8- and 4.2-kb mRNAs. The fact that the sizes of these mRNAs are similar to those of other ARFs (ARF 1, 1.9 kb; ARF 2, 2.6 kb; ARF 3, approximately 3.8 and 1.3 kb; ARF 4, 1.8 kb) explain the previously observed inconsistencies between the cDNA and ARF-specific oligonucleotide hybridization patterns. All six ARF cDNAs are more similar to each other than to other approximately 20-kDa guanine nucleotide-binding proteins.

ADP-Ribosylation Factor 6↗