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Biomedical subjects

A Greco

Publications and source records attributed to A Greco.

At least 73 records · Page 4Linked to original sources
PubMed1997

Repression of beta-actin synthesis and persistence of ribosomal protein synthesis after infection of HeLa cells by herpes simplex virus type 1 infection are under translational control.

Synthesis and assembly of ribosomal proteins into mature ribosomes persist late after infection of cells with herpes simplex virus type 1, while synthesis of beta-actin is drastically shut off. Since mRNAs encoding ribosomal proteins and beta-actin undergo concomitant degradation in infected HeLa cells, we have advanced the hypothesis that translation of the remaining mRNAs is differentially controlled after infection. The behaviour of mRNAs for three ribosomal proteins and for beta-actin was investigated during the course of infection. In uninfected cells, beta-actin mRNAs are associated with large polyribosomes, while only a part of ribosomal protein mRNAs are present in polyribosomes. In the course of infection, beta-actin mRNAs are released from the ribosomes and are sequestered with 40S ribosomal subunits. Simultaneously, ribosomal protein mRNAs become associated with an increased number of ribosomes, even late in infection. In addition, virally induced phosphorylation of ribosomal protein S6 is more efficient in pre-existing ribosomes than in newly assembled ribosomes. These results indicate that in infected cells (i) translation of beta-actin mRNA is selectively inhibited at a step necessary for binding the 60S ribosomal subunits; (ii) the rate of initiation of translation of ribosomal protein mRNAs increases after infection; and (iii) it is likely that translation of ribosomal protein mRNAs takes place preferentially on pre-existing ribosomes.

Actins↗
PubMed1997

The 3' untranslated region of the B19 parvovirus capsid protein mRNAs inhibits its own mRNA translation in nonpermissive cells.

Although parvoviruses are found throughout the animal kingdom, only the human pathogenic B19 virus has so far been shown to possess a limited host range, with erythroid progenitor cells as the main target cells supporting B19 propagation. The underlying mechanism of such erythroid tropism is still unexplained. Synthesis of the NS1 nonstructural protein occurs in permissive and nonpermissive cells, such as megakaryocytes, whereas synthesis of the VP1 and VP2 capsid proteins seems to be restricted to burst-forming units and CFU of erythroid cells. In nonpermissive cells, the NS1 protein is overexpressed and the NS1 RNAs are the predominant RNA species. However, the VP1 and VP2 proteins are not detectable, although the corresponding mRNAs are synthesized. Since all transcripts have part of the 5' untranslated region (5' UTR) in common but distinct 3' UTRs characterizing the nonstructural- and structural-protein mRNAs, we investigated, in transient transfection assays, the possible involvement of the 3' UTR of the capsid protein mRNAs in VP1 and VP2 protein synthesis in nonpermissive Cos cells. The results showed that (i) the 3' UTR of mRNAs coding for the capsid proteins repressed VP1 and VP2 protein synthesis, (ii) the 3' UTR did not affect nuclear export or mRNA stability, and (iii) mRNAs bearing the 3' UTR of the capsid protein mRNAs did not associate with ribosomes at all. Taken together, these results indicate that in nonpermissive cells, the 3' UTR of the capsid protein mRNAs represses capsid protein synthesis at the translational level by inhibiting ribosome loading.

Animals↗
PubMed1997

Helical CT angiography in gastrointestinal bleeding of obscure origin.

OBJECTIVE: The aim of the study was to verify the usefulness of helical CT angiography for diagnosis of gastrointestinal hemorrhage of obscure origin. SUBJECTS AND METHODS: Eighteen consecutive patients underwent catheterization of the abdominal aorta followed by helical CT angiography before and after intraarterial injections of a contrast medium. Helical CT angiography revealed the site of hemorrhage as an extravasation of contrast medium resulting in a hyperdense area in the intestinal lumen. All patients then underwent conventional angiography that was selective for the 13 patients in whom helical CT angiography was positive and standard for the remaining five patients with negative helical CT angiograms. RESULTS: Helical CT angiography revealed the site of hemorrhage in 13 (72%) of 18 patients. Diagnosis of bleeding site was confirmed, and the cause was established at surgery in 11 of these 13 patients. The site of bleeding for the remaining two patients was confirmed by angiography as angiodysplasia of the jejunum (n = 1) and of the colon (n = 1). Of the five patients with negative helical CT angiograms, location of bleeding was revealed by conventional angiography in two patients; one of the remaining three patients underwent exploratory laparotomy; and bleeding ceased in the remaining two patients, who were treated without surgery. Conventional angiography was negative for two of the 13 patients in whom helical CT angiography was positive. CONCLUSION: Despite our limited experience, helical CT angiography proved to be an easier and faster technique than conventional angiography for localizing gastrointestinal bleeding of obscure origin and useful as a guide for subsequent selective conventional angiography.

Adult↗
PubMed1997

Chromosome 1 rearrangements involving the genes TPR and NTRK1 produce structurally different thyroid-specific TRK oncogenes.

The NTRK1 gene in the q arm of chromosome 1 encodes one of the receptors for the nerve growth factor and is frequently activated as an oncogene in papillary thyroid carcinomas. The activation is due to chromosomal rearrangements juxtaposing the NTRK1 tyrosine kinase domain to 5'-end sequences from different genes. The thyroid TRK oncogenes are activated by recombination with at least three different genes: the gene coding for tropomyosin and TPR, both on chromosome 1,and TFG on chromosome 3. In a previous study, we showed that two tumors carrying the TPR/NTRK1 rearrangement contained structurally different oncogenes named TRK-T1 and TRK-T2. In this paper, we report (1) the cDNA structure of TRK-T2, (2) evidence that TRK-T2 is generated by different rearrangements in two thyroid tumors, and (3) a detailed analysis of the three different TPR/NTRK1 rearrangements. With molecular studies based on Southern blot hybridization, cloning, and sequencing, we show that all the rearrangements are nearly balanced, involving deletion, insertion, or duplication of only few nucleotides. In one case, an additional rearrangement involving sequences derived from chromosome 17 was detected.

Base Sequence↗
PubMed1997

Brain MR in chronic fatigue syndrome.

PURPOSE: To determine the prevalence of MR white matter abnormalities in patients with chronic fatigue syndrome (CFS). METHODS: Brain MR studies of 43 patients (29 women and 14 men, 22 to 78 years old) with a clinical diagnosis of CFS (n = 15), CFS with associated depression (n = 14), and CFS with associated other psychiatric disorders, namely, anxiety and somatization disorder (n = 14), were compared with brain MR studies in 43 age- and sex-matched control subjects. RESULTS: MR findings were abnormal in 13 (32%) of the patients in the study group (ages 34 to 78 years) and in 12 (28%) of the control subjects (ages 26 to 73 years). One patient with CFS had multiple areas of demyelination in the supratentorial periventricular white matter. Another patient with CFS and associated depression had a single focus of probable demyelination in the supratentorial periventricular white matter. In four patients with CFS (ages 34 to 48 years) MR abnormalities consisted of one or several punctate hyperintense foci in the corona radiata, centrum ovale, and frontal white matter. The remaining seven patients (ages 50 to 78 years) had frontoparietal subcortical white matter foci of high T2 signal. The prevalence of white matter hyperintensities was not different between the patients and the control subjects. CONCLUSIONS: Our findings suggest that no MR pattern of white matter abnormalities is specific to CFS.

Adult↗
PubMed1997

Prothrombin synthesis in the adult and fetal liver.

Plasma levels of blood coagulation zymogens are lower in the newborn than in the adult, with the lowest levels being in preterm infants. It is not known if the lower coagulation factor levels reflect differences in synthesis, secretion or catabolism. Using a rabbit model we have compared prothrombin synthesis in the fetus and adult. In previous studies we attempted to compare transcription in the adult and fetal liver by extraction of mRNA, immobilization on a membrane and hybridization with a labeled cDNA for rabbit prothrombin. Comparison was impaired by the markedly dissimilar composition of fetal and adult rabbit liver; fetal liver is approximately fifty percent hematopoietic tissue even at term (1). In the present study, to obtain a more meaningful comparison we have employed in situ hybridization to compare directly prothrombin expression in adult and fetal liver. We report here that fetal liver contains more prothrombin mRNA than does adult liver. We have further compared prothrombin levels in protein extracts of adult and fetal liver and found that per microgram of extract, fetal liver contains as much prothrombin as does the adult. We conclude that the lower plasma prothrombin levels in the fetus do not reflect a lower rate of synthesis.

Animals↗
PubMed1996

Genomic organization of the human NTRK1 gene.

The NTRK1 gene encodes one of the receptors for the Nerve Growth Factors and it is located at 1q21-22. Rearrangements of NTRK1 are frequently detected in human papillary thyroid carcinoma and lead to the formation of chimeric oncogenes, similarly to what observed for the other neurotrophin receptor RET. In addition, the two receptor genes are target of point mutations associated with different human diseases. RET is affected by germ line and somatic mutations in MEN2A, MEN2B tumor syndromes and in the abnormal developmental Hirschsprung disease, whereas mutations of NTRK1 have been reported very recently in patients with congenital insensitivity to pain with anidrosis (CIPA). With the aim to provide a tool for searching mutations along the whole NTRK1 gene, we have determined its genomic organization. Our results demonstrated that NTRK1 is contained within 25 Kb of DNA and is organized in 17 exons, one of which is alternatively spliced. The sequence of the 5' flanking region indicates a high content in C/G, the absence of TATA box, the presence of several putative binding sites for Sp1, AP1, AP2, AP3, ATF and GCF transcription factors.

Alternative Splicing↗
PubMed1996

Cytogenetics and molecular genetics of carcinomas arising from thyroid epithelial follicular cells.

Cytogenetic and molecular analyses of thyroid tumors have indicated that these neoplasms represent a good model for analyzing human epithelial cell multistep carcinogenesis. They comprise, in fact, a broad spectrum of lesions with different phenotypes and variable biological and clinical behavior. Molecular analysis has detected specific genetic alterations in the different types of thyroid tumors. In particular, the well-differentiated carcinomas of the papillary type are characterized by activation of the receptor tyrosine kinases (RTKs), RET and NTRK1 proto-oncogenes. Cytogenetic analysis of these tumors has contributed to defining the chromosomal mechanisms leading to RTK oncogenic activation. In the majority of cases, intrachromosomal inversions of chromosome 10 and chromosome 1 led to the formation of RET-derived and NTRK1-derived oncogenes, respectively. Interestingly, molecular analysis of these oncogenes revealed their nature of chimeric fusion proteins all sharing the tyrosine kinase (TK) domains of the respective proto-oncogenes. Moreover, the sequencing of the oncogenic rearrangements led to the identification of a breakpoint cluster region in both RTK proto-oncogenes. Exposure to ionizing radiation is associated with papillary carcinomas and RET activation has been suggested to be related to this event. Conversely, RAS point mutations are frequently observed in tumors with follicular histology and have been associated with metastatic dissemination. Iodide-deficient areas seem to provide a higher frequency of RAS positive follicular carcinomas. Finally, a high prevalence of TPS3 point mutations has been detected only in undifferentiated or anaplastic carcinomas and found to correlate inversely with 8CL2 expression. All of these findings are contributing to the definition of genetic and environmental factors relevant for the pathogenesis of thyroid tumors. Moreover, the characterization of specific genetic lesions could provide significant molecular tools for a better differential diagnosis and for the development of novel therapeutic avenues for thyroid cancer.

Carcinoma, Papillary↗
PubMed1996

Induction of prostaglandin endoperoxide synthase-2 in human monocytes associated with cyclo-oxygenase-dependent F2-isoprostane formation.

1. The isoprostane 8-epi-prostaglandin (PG)F2 alpha is produced by free radical-catalyzed peroxidation of arachidonic acid. It may also be formed as a minor product of the cyclo-oxygenase activity of platelet PGH synthase (PGHS)-1. We investigated 8-epi-PGF2 alpha production associated with induction of the human monocyte PGHS-2 and its pharmacological modulation. 2. Heparinized whole blood samples were drawn from healthy volunteers, 48 h following oral dosing with aspirin 300 mg to suppress platelet cyclo-oxygenase activity. One ml aliquots were incubated with lipopolysaccharide (LPS: 0.1-50 micrograms ml-1) for 0-24 h at 37 degrees C. PGE2 and 8-epi-PGF2 alpha were measured in separated plasma by radioimmunoassay and enzyme immunoassay techniques. 3. Levels of both eicosanoids were undetectable (i.e. < 60 pg ml-1) at time 0. LPS induced the formation of PGE2 and 8-epi-PGF2 alpha in a time- and concentration-dependent fashion, coincident with the induction of PGHS-2 detected by Western blot analysis of monocyte lysates. After 24 h at 10 micrograms ml-1 LPS, immunoreactive PGE2 and 8-epi-PGF2 alpha averaged 10,480 +/- 4,643 and 295 +/- 140 pg ml-1 (mean +/- s.d., n = 6), respectively. 4. Dexamethasone and 5-methanesulphonamido-6-(2,4-difluorothiophenyl)-1-indano ne (L-745,337), a selective inhibitor of the cyclo-oxygenase activity of PGHS-2, reduced PGE2 and 8-epi-PGF2 alpha production in response to LPS. 5. Isolated monocytes produced PGE2 and 8-epi-PGE2 alpha in response to LPS (10 micrograms ml-1) in a time-dependent fashion. Monocyte PGE2 and 8-epi-PGF2 alpha production was largely prevented by dexamethasone (2 microM) and cycloheximide (10 micrograms ml-1) in association with suppression of PGHS-2 but not of PGHS-1 expression. 6. We conclude that the induction of PGHS-2 in human monocytes is associated with cyclo-oxygenase-dependent generation of the vasoconstrictor and platelet-agonist 8-epi-PGF2 alpha.

Adult↗
PubMed1996

Computed tomography visceral adipose tissue volume measurements of Italians. Predictive equations.

OBJECTIVES: To evaluate total visceral adipose tissue (AT) volumes in relation to single slices of visceral AT area measured at different levels and to other simple anthropometric measurements. DESIGN: Only outpatients examined in a metabolic unit were considered; subjects without conditions known to affect AT distribution who gave their informed consent were recruited. SETTING: All subjects were hospitalized in the Department of Internal Medicine of the University of Messina. SUBJECTS: 90 adult subjects of which 18 men and 42 pre- and 30 post-menopausal women. Ages ranged from 18 to 69 years and body mass indexes ranged from 22 to 50. INTERVENTIONS: The AT volume was calculated by computed tomography from the AT area of five scans and from the distances between these scans. RESULTS: AT area at the level of the 2nd-3rd lumbar vertebra had by itself the highest predictive power in men (s.e. = 6.8%), in post-menopausal women (s.e. = 7.4%) and, together with age, in pre-menopausal women (s.e. = 14%). Of the non-radiological parameters it was waist circumference, together with age, which showed the highest predictive power in men (s.e. = 21%), pre-menopausal women (s.e. = 25%) and, together with height, in post-menopausal women (s.e. = 33%). CONCLUSIONS: A single scan measurement at the lumbar level was confirmed to be representative of total visceral AT volume. Waist circumference was the non-radiological parameter that best correlated with volume.

Adipose Tissue↗
PubMed1995

RET activation by germline MEN2A and MEN2B mutations.

The RET proto-oncogene encodes a receptor tyrosine kinase (TK). It has been shown that distinct germline mutations in the RET proto-oncogene are associated with the dominantly inherited cancer syndromes multiple endocrine neoplasia type 2A and 2B (MEN 2A and MEN 2B) and familial medullary thyroid carcinoma (FMTC) as well as Hirschsprung disease (HSCR), a congenital disorder characterised by absent enteric innervation. In this study, we have transfected NIH3T3 and PC12 phaeochromocytoma cells with MEN2A (Cys634-> Arg) and MEN2B (Met918-> Thr) RET constructs. Both caused transformation of the NIH3T3 cells and differentiation of PC12 cells. The Ret (MEN2A) and Ret (MEN2B) proteins were constitutively phosphorylated on tyrosine, and their in vitro kinase activity was significantly higher than that of the wild type protein. The MTC cell line TT carries a CYs634-> Trp MEN2A mutation, and we have shown by immunoelectronmicroscopy that Ret is clustered on the cell surface in a manner reminiscent of ligand-induced aggregation of cell surface receptors. RET is activated, as RET/PTC oncogene, by somatic rearrangements which link the TK domain to a constitutive dimerization interface in papillary thyroid carcinomas. We have compared the biological and biochemical activity of the TK domains of the wild type and MEN 2B Ret in the context of the RET/PTC. The results show that the MEN 2B mutation significantly increases the TK domain enzymatic activity suggesting that dimerization may be still necessary for MEN 2B Ret to express its full activity.

3T3 Cells↗
PubMed1995

Oncogenic rearrangements of the RET proto-oncogene in papillary thyroid carcinomas from children exposed to the Chernobyl nuclear accident.

Since the Chernobyl nuclear reactor accident, a striking increase of thyroid carcinoma has been reported in children exposed to radiation in Belarus. Because of its unprecedented scale and its emotional implications, this finding has raised concern and called the attention of the scientific community to this major health problem. Although epidemiologically documented, a direct correlation between thyroid cancer and radiation exposure has not been definitely proven at the molecular level. On the assumption that ionizing radiation could cause specific and common cancer-associated genetic lesions, an analysis of oncogene activation and/or tumor suppressor gene inactivation would help to define radiation-induced thyroid carcinomas. Therefore, we have analyzed by different molecular approaches, including Southern blotting, DNA transfection assay on NIH-3T3 cells, and reverse transcription-PCR analysis, six papillary carcinomas from children living in the region of Belarus at the time of the Chernobyl nuclear accident to identify tumor-specific gene rearrangements of the proto-oncogenes RET and TRK, previously found activated in a tumor type-specific manner in papillary thyroid carcinoma. Using Southern blot analysis in four cases, we could detect specific rearranged bands indicating an oncogenic activation of RET that in three cases resulted in rearranged sequences provided by the same activating gene. Moreover, the DNA of the last three cases showed a biological activity in transforming NIH-3T3 cells after the DNA-mediated transfection assay, and the respective NIH-3T3 transfectants were found to express the oncogenic fusion transcripts. These results support the possibility that RET oncogenic activation could represent a major genetic lesion associated with thyroid carcinoma in children exposed to the Chernobyl nuclear accident.

3T3 Cells↗
PubMed1995

A phase I study of etoposide phosphate administered as a daily 30-minute infusion for 5 days.

PURPOSE: To determine the maximum tolerated dose, toxicities, kinetics, and disposition of etoposide phosphate when administered as a daily 30-minute infusion for 5 days. PATIENTS AND METHODS: Twenty-eight patients were enrolled in this phase I dose-escalation trial. Cohorts of patients received etoposide phosphate in etoposide equivalent doses of 50, 75, 100 and 125 mg/m2 intravenously for 30 minutes each day for 5 days. Pharmacokinetic sampling of both blood and urine was performed and concentrations of etoposide and etoposide phosphate were determined on day 1 of study for each patient and on day 4 of study for three patients receiving the 100 mg/m2 dose. RESULTS: The dose-limiting toxicity was reversible myelosuppression as evidenced by leukopenia and neutropenia. Toxicities seen were comparable to those expected from etoposide administration. With this schedule, the 100 mg/m2 dose was the maximum tolerated dose. Nonhematologic toxicities were generally mild. Two patients had major responses and three others had minor responses. Pharmacokinetic analyses revealed rapid (< 15 minutes) extensive conversion of etoposide phosphate to etoposide. Peak plasma etoposide concentrations and etoposide areas under the curve were proportional to the dose of etoposide phosphate administered. Etoposide kinetics were similar to those expected after a comparable dose of etoposide. CONCLUSIONS: Etoposide phosphate is a water-soluble pro-drug of etoposide that is rapidly converted to etoposide in vivo with a toxicity profile similar to etoposide. Etoposide generated from etoposide phosphate exhibits linear kinetics over a dose range of 50 to 125 mg/m2. When administered as a daily 30-minute infusion for 5 days, the dose-limiting toxicity is myelosuppression and 100 mg/m2 daily is the maximum tolerated dose.

Adult↗
PubMed1995

Effects of nabumetone on prostanoid biosynthesis in humans.

BACKGROUND: The active metabolite of the anti-inflammatory drug nabumetone has been characterized as a selective inhibitor of the inducible prostaglandin H synthase (PGHS). The aim of this study was to investigate the rate of eicosanoid biosynthesis after oral dosing with nabumetone in nine healthy subjects. METHODS: We measured the urinary excretion of products of platelet (11-dehydro-thromboxane B2 [TXB2]) and renal (prostaglandin IF2 alpha [PGF2 alpha]) arachidonate metabolism as in vivo indexes of the constitutive PGHS-1 pathway. Moreover, the production of TXB2 during whole blood clotting was assessed as an index of the cyclooxygenase activity of platelet PGHS-1 ex vivo. RESULTS: At steady state, nabumetone (500 and 1000 mg daily for 7 days) was associated with statistically significant dose-dependent reduction in the urinary excretion of 11-dehydro-TXB2 and serum TXB2 levels by approximately 50% to 70%. However, the drug did not significantly affect the urinary excretion of PGF2 alpha. After discontinuation of nabumetone, urinary 11-dehydro-TXB2 excretion and whole blood TXB2 production returned to predrug levels with a similar timecourse that was consistent with the elimination half-life of its active metabolite. The daily administration of low-dose aspirin (40 mg), a selective inhibitor of platelet PGHS-1, caused a cumulative inhibition of urinary 11-dehydro-TXB2 and whole blood TXB2 production that recovered with a timecourse consistent with platelet turnover. CONCLUSIONS: Nabumetone does dose-dependently inhibit the cyclooxygenase activity of platelet PGHS-1 of healthy subjects both in vivo and ex vivo. Thus it is unlikely that its safety profile in patients may be related to selective inhibition of the inducible PGHS-2.

Administration, Oral↗
PubMed1995

Loss of function effect of RET mutations causing Hirschsprung disease.

We have introduced three Hirschsprung (HSCR) mutations localized in the tyrosine kinase domain of RET into the RET/PTC2 chimaeric oncogene which is capable of transforming NIH3T3 mouse fibroblasts and of differentiating pC12 rat pheochromocytoma cells. The three HSCR mutations abolished the biological activity of RET/PTC2 in both cell types and significantly decreased its tyrosine phosphorylation. By contrast, a rare polymorphism in exon 18 does not alter the transforming capability of RET/PTC2 or its tyrosine phosphorylation. These data suggest a loss of function effect of HSCR mutations which might act through a dominant negative mechanism. Our model system is therefore capable of discriminating between causative HSCR mutations and rare polymorphisms in the tyrosine kinase domain of RET.

3T3 Cells↗
PubMed1995

Effects of the novel anti-inflammatory compounds, N-[2-(cyclohexyloxy)-4-nitrophenyl] methanesulphonamide (NS-398) and 5-methanesulphonamido-6-(2,4-difluorothio-phenyl)-1-inda none (L-745,337), on the cyclo-oxygenase activity of human blood prostaglandin endoperoxide synthases.

1. We have evaluated the selectivity of ketoprofen and two novel nonsteroidal anti-inflammatory drugs, N-[2-(cyclohexyloxy)-4-nitrophenyl]methanesulphonamide (NS-398) and 5-methanesulphonamido-6-(2,4-difluorothiophenyl)-1-indano ne (L-745,337), in inhibiting the cyclo-oxygenase activity of prostaglandin endoperoxide synthase-2 (PGHS-2) vs PGHS-1 in human blood monocytes and platelets, respectively. 2. Heparinized whole blood samples were drawn from healthy volunteers pretreated with aspirin, 300 mg 48 h before sampling, to suppress the activity of platelet PGHS-1 and incubated at 37 degrees C for 24 h with increasing concentrations of the test compounds in the presence of lipopolysaccharide (LPS, 10 micrograms ml-1). Immunoreactive PGE2 levels were measured in plasma by a specific radioimmunoassay as an index of the cyclo-oxygenase activity of LPS-induced monocyte PGHS-2. 3. The effects of the same inhibitors on platelet PGHS-1 activity were assessed by allowing whole blood samples, drawn from the same subjects in aspirin-free periods, to clot at 37 degrees C for 1 h in the presence of the compounds and measuring immunoreactive thromboxane B2 (TXB2) levels in serum by a specific radioimmunoassay. 4. Under these experimental conditions, ketoprofen enantioselectively inhibited the cyclo-oxygenase activity of both PGHS-1 and PGHS-2 with equal potency (IC50 ratio: approx. 0.5 for both enantiomers), while L-745,337 and NS-398 achieved selective inhibition of monocyte PGHS-2 (IC50 ratio: > 150). L-745,337 and NS-398 did not affect LPS-induced monocyte PGHS-2 biosynthesis to any detectable extent. 5. We conclude that L-745,337 and NS-398 are selective inhibitors of the cyclo-oxygenase activity of human monocyte PGHS-2. These compounds may provide adequate tools to test the contribution of this novel pathway of arachidonate metabolism to human inflammatory disease.

Adult↗