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Biomedical subjects

M R Jones

Publications and source records attributed to M R Jones.

At least 109 records · Page 6Linked to original sources
PubMed1992

Stimulation of early gene expression by angiotensin II in bovine adrenal glomerulosa cells: roles of calcium and protein kinase C.

The adrenal glomerulosa cell is a major site of action of angiotensin II (AII), which binds to AT1 receptors to stimulate phosphoinositide hydrolysis and Ca2+ mobilization, and the subsequent production of aldosterone. All also influences adrenal growth and proliferation and promotes thymidine incorporation in adrenocortical cells. In primary cultures of bovine glomerulosa cells, AII was found to induce the expression of several early growth response genes (c-fos, c-jun, JunB, and Krox 24). This effect of AII was dose-dependent and was blocked by [Sar1,IIe8] AII and the nonpeptide antagonist DuP 753, indicating that it is mediated by the AT1 subtype of the AII receptor. ACTH, which elevates cAMP in glomerulosa cells, was a relatively weak inducer of c-fos expression but was as potent as AII in stimulating the expression of JunB. ACTH did not further enhance the maximal effect of AII on c-fos expression. The role of the AII-induced cytoplasmic Ca2+ increase in generating the c-fos response was suggested by the ability of the Ca2+ ionophore ionomycin to induce c-fos expression. However, mobilization of intracellular Ca2+ by the Ca2+ ATPase inhibitor thapsigargin, as well as the stimulation of Ca2+ influx by depolarization with potassium, were less potent stimuli of c-fos expression. Omission of Ca2+ from the extracellular medium, which abolishes the plateau phase of the AII-induced Ca2+ signal without affecting the early increase due to Ca2+ mobilization, enhanced the early phase of the AII-induced c-fos response, indicating that Ca2+ also has an inhibitory effect on the early gene response. Activation of protein kinase C by phorbol 12-myristate, 13-acetate (PMA) also stimulated c-fos expression, but the combination of PMA and ionomycin did not further increase the c-fos response. Inhibition of protein kinase C by staurosporine, or its depletion by prolonged exposure to PMA, prevented the c-fos response to PMA but only partially inhibited the response to AII, suggesting the involvement of other factors in stimulus-transcription coupling from the AT1 receptor.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1992

Passive immunization with antiserum to adrenocorticotropin increases weight gain in normal female rats.

Passive immunization against ACTH was used to test the hypothesis that growth in female rats is constrained by physiological concentrations of glucocorticoids. When animals were stressed by 15-min exposure to ether before blood sampling by cardiac puncture, serum concentrations of corticosterone were lower (P less than .05) in immunized rats than in stressed controls. The maximum effect was apparent 2 h after injection of ACTH antiserum, and no effect was apparent 6 h after injection. To examine the effects of ACTH immunization on growth, rats received daily injections of either saline, sheep immunoglobulin G, or ACTH antiserum, 2 h before the afternoon peak in plasma concentrations of corticosterone. After 7 d of treatment, rats treated with ACTH antiserum had gained 37% more body weight than saline-injected controls, and this effect was accompanied by a 59% reduction in peak plasma concentrations of corticosterone. Immunoglobulin G purified from normal sheep serum had no effect on weight gain. It is concluded that growth rate in normal female rats can be stimulated through the suppression of adrenal activity.

Adrenocorticotropic Hormone↗
PubMed1992

The development of corticosteroid binding globulin-like activity in fetal sheep blood.

Parturition in sheep is initiated by the fetus and is preceded by a rise in fetal cortisol and corticosteroid-binding globulin (CBG) late in gestation. In this study plasma cortisol and CBG concentrations were measured in fetal and maternal circulation from 40 days gestation to early post-partum. The fetal cortisol profile was shown to be triphasic in nature; being high in both the first and last trimester but low in the middle period of gestation. In the last trimester, total cortisol increased steadily, reaching it's highest level just prior to parturition (145 days gestation), before falling to maternal levels over the first 10 days post-partum. The changes seen in CBG concentrations throughout gestation and post-partum mirrored the triphasic nature seen in cortisol levels. CBG was significantly higher at 40, 56 and 140 days gestation than at mid-gestation (77 and 90 days). However, at 145 days gestation there was a significant fall in CBG levels. CBG levels were higher at 1 day post-partum when compared to 145 days gestation, the former rapidly falling to maternal levels over the subsequent 9 days. The maximum binding capacity at 40, 56, 70 and 90 days gestation exceeds the total serum cortisol concentration. However at 140 and 145 days gestation and 1 day post-partum the total serum cortisol exceeds the Bmax. The highest cortisol:Bmax ratio is seen at 145 days gestation due to the fall of CBG binding capacity at this time.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

Amino acid solutions for CAPD: rationale and clinical experience.

Protein-calorie malnutrition is present in a sizable proportion of dialysis patients. In CAPD patients, constant glucose absorption from dialysate may displace other calorie sources, such as protein, and may suppress the appetite, thus contributing to malnutrition. Use of amino acids in place of glucose as the osmotic agent has been studied extensively. Ultrafiltration and small-molecule clearance similar to that with glucose can be achieved with amino acid solutions, but nitrogenous waste produced by amino acids limits the extent to which they can replace hypertonic glucose. Side effects of CAPD with amino acids appear to be minor and easily manageable. Most studies have found at least some nutritional benefit of amino acid solutions in addition to that of lowering the glucose load. Short-term studies of amino acid solutions for dialysis indicate that they may improve protein nutrition in malnourished CAPD patients.

Amino Acids↗
PubMed1991

Effects of poloxamer 188 on the assembly, structure and dissolution of fibrin clots.

Poloxamer 188, N.F. (RheothRx), a nonionic block copolymer composed of 2 hydrophilic polyoxyethylene chains connected by a hydrophobic polyoxypropylene chain, normalizes the viscosity of whole blood high in soluble fibrin(ogen) complexes. Normalization may be via a poloxamer 188-induced decrease in fibrin(ogen)-red cell interaction. Our study examined the influences of poloxamer 188 on fibrin assembly and structure. Studies were performed in both purified and plasma systems with a poloxamer 188 concentration range of 0.1-20 mg/ml and specific clotting conditions (fibrinogen 1 mg/ml, thrombin 1 NIH u/ml, pH 7.4 [Tris 0.05 M], ionic strength 0.15 and calcium 5 mM). Fibrin assembly was accelerated in the presence of poloxamer 188. As poloxamer 188 concentration was increased from 0 to 8 mg/ml in plasma: a) the lag phase prior to initial turbidity rise decreased from 25 to less than 5 s; b) the final gel optical density (OD) increased from 0.65 to 1.28 and c) fiber size (mass/length ratio [mu]) increased from 4.3 to 12.6 x 10(13) daltons/cm. Similar results were seen in the purified system with a poloxamer 188 concentration range of 0-8 mg/ml. OD increased from 0.26 to 0.51, and mu increased from 2.3 to 5.3 x 10(13) daltons/cm. Above 8 mg/ml, precipitation of fibrinogen was noted in this system. Since large fibrin fibers tend to be degraded more rapidly, possible poloxamer mediated enhancement of r-tPA-mediated clot lysis was investigated. With r-tPA (70 lu/ml) present at the time of clotting, clot lysis in the presence of ploxamer 188 (8 mg/ml) was 50% complete at 1,600 s compared to 2,540 s for the control. Thus, poloxamer 188-induced alterations in fibrin structure and fibrin-cell interactions may explain some of this agent's interesting hemorrheologic and antithrombotic properties.

Blood Coagulation↗
PubMed1991

The use of prophylactic eye drops during high-dose cytosine arabinoside therapy.

An ocular toxic reaction presenting as conjunctivitis or keratitis develops in a significant number of patients who are treated with high-dose cytosine arabinoside (ara-C). Although eye drops containing glucocorticoid reportedly decrease the incidence, they do not totally eliminate this side effect. In comparing this technique with artificial tears, both were found to be equally effective. The primary mechanism by which eye drops decrease ocular toxic reactions associated with high-dose ara-C is presumably due to dilution of intraocular concentrations of ara-C.

Adult↗
PubMed1991

Retroconversion and delta 4 desaturation of docosatetraenoate (22:4(n-6)) and docosapentaenoate (22:5(n-3)) by human cells in culture.

This study has investigated the metabolic modification of [3-14C]docosatetraenoate (22:4(n-6)) and [3-14C]docosapentaenoate (22:5(n-3)) by human cells in culture. Fetal skin fibroblasts converted as much as 20% of the incorporated [14C]22:4(n-6) to [14C]20:4(n-6) within 6 h and 41% within 48 h. Retroconversion of incorporated [14C]22:5(n-3) was less than 13% at all time points. Chain shortening of [14C]22:4(n-6) was also 2-6-fold greater than that of [14C]22:5(n-3) in retinoblastoma and vascular endothelial cells. Fibroblasts, vascular endothelial cells and retinoblastoma cells all elongated substantially more [14C]eicosapentaenoate than [14C]arachidonate to the respective C22 fatty acids. Within 3-4 days, fibroblasts incubated with either [14C]20:5(n-3) or [14C]22:5(n-3) had the same ratio of radiolabeled C22:C20 fatty acids in cellular glycerolipids. By contrast, the cells incubated with [14C]22:4(n-6) or [14C]20:4(n-6) did not reach a common C22/C20 equilibrium by 5 days. Although fibroblasts were found to desaturate [14C]22:5(n-3), a substantial lag time was observed; [14C]22:6(n-3) was 2% at 48 h and 20% at 96 h. By contrast, synthesis of [14C]22:6(n-3) by retinoblastoma cells was 51% within 6 h and greater than 90% at 96 h. Desaturation of [14C]22:4(n-6) was observed in retinoblastoma cells, but not in fibroblasts. These results thus suggest that the ratio of C22C20 polyunsaturated fatty acids in cells is regulated by the relative rates of retroconversion and chain elongation, with the net effect of the two processes favoring C20 for n-6 and C22 for the n-3 fatty acids. Furthermore, although fibroblasts desaturate [14C]22:5(n-3), the process appears to be qualitatively different from that of retinoblastoma cells.

Animals↗
PubMed1991

Magnesium absorption: mechanisms and the influence of vitamin D, calcium and phosphate.

Magnesium absorption has been studied in both humans and animals under diverse experimental conditions. As a result, the data often appear confusing and conflicting. In this review we attempt to summarize information concerning Mg absorption and, where possible, to reconcile apparently conflicting observations. Most studies suggest that Mg is absorbed predominantly in the distal intestine. At usual Mg intakes, Mg absorption occurs primarily by intercellular diffusional and solvent drag mechanisms. There is evidence for a saturable component of Mg absorption in the small intestine and the descending colon that is important at low dietary Mg intakes. Pharmacological doses of vitamin D increase Mg absorption in both vitamin D-deficient and vitamin D-replete animals. A substantial amount of Mg absorption, however, occurs independent of vitamin D. In addition, vitamin D may reduce Mg retention through increases in urinary Mg excretion. Intestinal interactions between Mg and calcium or phosphate have been demonstrated in both humans and animals. The nature of these interactions cannot be readily explained by data currently available.

Animals↗
PubMed1991

Platelet and fibrin modification by radiographic contrast media.

The effect of the radiographic contrast agents, iopamidol and diatrizoate, on fibrin assembly and structure as well as platelet surface charge was studied. Increasing the iopamidol concentration from 0 to 4.5 mM prolongs the fibrin gelation time from 20 to 105 seconds (an anticoagulant effect) and reduces the fibrin fiber mass/length ratio from 3.2 x 10(12) to 0.5 x 10(12) Da/cm (i.e., produces very thin fibrin fibers). Ultraviolet difference spectroscopy of fibrinogen showed both a 15-nm shift in the ultraviolet difference maximum for iopamidol (suggesting binding) and a perturbation of the aromatic amino acid side chain region for fibrinogen (suggesting a conformational change in fibrinogen) as the concentration of iopamidol was increased from 0 to 9 mg/ml. Binding of iopamidol to fibrinogen was also shown by affinity chromatography using a Sepharose-fibrinogen column. Electrophoretic quasi elastic light scattering was used to show platelet interaction with iopamidol as reflected in a reduction in the platelet electrophoretic mobility from 2.0 to 0.5 (microns-cm)/(V-sec) as the concentration of iopamidol was increased from 0 to 4.5 mM. In addition, the ionic radiopaque contrast agent, Renografin, was also studied and found to inhibit fibrin monomer assembly. Although iopamidol is not shown to be thrombogenic, iopamidol does appear to reduce platelet surface charge, bind fibrinogen, and modify fibrin clot structure.

Blood Platelets↗
PubMed1991

Some influences of accent structure on melody recognition.

Two experiments were carried out to investigate the roles of joint accent structure and familiarity in delayed recognition of relatively long tonal melodies. Melodic themes of target melodies were defined by correlating contour-related pitch accents with temporal accents (accent coupling) during an initial familiarization phase. Later, subjects gave recognition responses to key-transposed versions of the target melodies as well as to decoys with same and different contour accent patterns. In Experiment 1, all to-be-recognized melodies occurred both in an original rhythm, which preserved accent coupling, and in a new rhythm, which did not. Listeners were best at distinguishing targets from different decoys, especially in the original rhythm. In Experiment 2, the familiarity of target tunes and the rhythmic similarity in recognition were varied. Similar rhythms preserved accent coupling, whereas dissimilar rhythms did not. Listeners were most adept in distinguishing familiar targets from different decoys (Experiment 2A), particularly when they appeared in novel but similar rhythms. However, in similar rhythm conditions, listeners also frequently mistook same decoys for targets. With less familiar targets (Experiment 2B), these effects were attenuated, and performance showed general effects of pitch contour.

Adult↗
PubMed1990

The role of c-type cytochromes in the photosynthetic electron transport pathway of Rhodobacter capsulatus.

(1) Short flash excitation of membrane vesicles of a cytochrome-c2-deficient mutant of Rhodobacter capsulatus (strain MT-G4/S4) led to rapid oxidation of a c-type cytochrome. In redox titrations, the photooxidation of c-type cytochrome was attenuated with a midpoint of approx. +360 mV. Vesicles from a control strain, MT1131, gave similar results. These findings are consistent with those of Prince et al. (Prince, R.C., Davidson, E., Haith, L.E. and Daldal, F. (1986) Biochemistry 25, 5208-5214). (2) In anaerobic intact cells the extent of rapid re-reduction of c-type cytochrome oxidised after a flash was less in MT-G/S4 than in MT1131. Cytochrome c reduction in both strains was inhibited by myxothiazol. The myxothiazol-sensitive component of the electrochromic absorbance change in cells indicated that rapid charge separation through the cytochrome bc1 complex was less extensive after a flash in MT-G4/S4 than in MT 1131. (3) In anaerobic intact cells and in chromatophores of Rb. capsulatus strain MT-GS18, a mutant deficient in both cytochrome c1 and cytochrome c2, flash excitation led to the oxidation of c-type cytochrome. Redox titrations and spectra of chromatophores suggested that this is the same cytochrome as was photooxidized in vesicles of MT-G4/S4 and MT1131. This result is in contrast with earlier findings (Prince, R.C. and Daldal, F. (1987) Biochim. Biophys, Acta 894, 370-378) in which it was reported that no photooxidation of c-type cytochrome occurred in the absence of c1 and c2, and argues against the possibility that cytochrome c1 can rapidly and directly donate electrons to the reaction centre. (4) It is proposed that a previously uncharacterized, membrane-bound c-type cytochrome (Em7 approximately +360 mV) is present in Rb-capsulatus MT1131, in the c2-deficient mutant MT-G4/34 and in the c1/c2-deficient mutant MTGS18. This cytochrome and cytochrome c2 are alternative electron donors to the reaction centre in strain MT1131.

Cytochrome c Group↗
PubMed1990

Comparison of calcium and magnesium absorption: in vivo and in vitro studies.

Transport characteristics of Ca and Mg were compared at three different levels of the absorptive process in male (120-170 g) Wistar rats. Balance studies in intact rats revealed that fractional Ca absorption decreased with increased Ca intake so that net Ca absorption remained constant. Fractional Mg absorption decreased modestly with increased Mg intake so that net Mg absorption increased proportionately with increased dietary Mg. Everted duodenal sacs demonstrated the presence of active Ca absorption with serosal-to-mucosal (S/M) ratio of 2.65 +/- 0.20 (n = 6), which was greater than unity (P less than 0.001). In contrast, the S/M for Mg did not exceed unity. Mucosal duodenal Ca uptake exhibited a large saturable (Michaelis constant of 4.80 +/- 0.34 mM, maximal velocity of 4.71 +/- 0.13 nmol.min-1.mg-1) and a small nonsaturable component (0.12 +/- 0.01 nmol.min-1.mg-1) in 5-wk-old rats (120 g). In 72-wk-old rats (600 g) the diffusional component of Ca uptake became predominant, and the slope increased significantly to 0.32 +/- 0.01 (P less than 0.05). Duodenal Mg uptake was completely concentration dependent and exhibited no age-related changes.

Animals↗
PubMed1990

Site and mechanism of intestinal magnesium absorption.

Despite considerable research on magnesium (Mg) absorption there is still uncertainty regarding the site and mechanism of intestinal Mg transport. A careful review of the literature indicates that while Mg is absorbed throughout the intestine, the predominate site is the distal small intestine. There are three mechanisms by which Mg has been shown to cross the intestine:passive diffusion, solvent drag, and active transport. The importance of each of these mechanisms to total Mg absorption is discussed. Studies in both humans and experimental animals indicate that passive diffusion through the paracellular pathway accounts for the majority of Mg absorbed. Investigators have also consistently demonstrated the existence of a saturable component. Studies in everted gut sacs, however, have failed to demonstrate that Mg is actively transported against a concentration gradient in young or adolescent rats. Recent studies using the Ussing chamber have documented that Mg is actively transported in the descending colon.

Animals↗
PubMed1989

The coupling between protonmotive force and the NAD(P)+ transhydrogenase in chromatophores from photosynthetic bacteria.

1. The activity of NAD(P)+ transhydrogenase in chromatophores of Rhodobacter capsulatus relaxed from a high rate during illumination to a lower rate after darkening with a half-time of approximately 100 ms. 2. The dissipative ionic current flowing across the chromatophore membrane was increased in the presence of transhydrogenase substrates. This is attributed to proton current through the transhydrogenase enzyme. Subject to the assumption that transhydrogenase does not conduct in the absence of nucleotide substrates, the ratio of protons translocated across the membrane per hydride ion transferred was 0.4 +/- 0.5. Within the error and uncertainities in the calibration procedure, this ratio may be consistent with a stoichiometry of one but higher values seem unlikely. The ratio of hydride ion transferred in the transhydrogenase to electrons transferred through the cyclic electron transport system was approximately 0.2. 3. The Kappm values for the transhydrogenase substrates were determined for chromatophores in illuminated and darkened suspensions over a range of pH. These values are discussed in relation to the equivalent parameters reported for mitochondria transhydrogenase [Rydstrom, J. (1977) Biochim. Biophys. Acta 255, 9641-9646] and were used to calculate the concentrations of substrates which effectively saturate the enzyme. 4. At substrate concentrations which were in excess of 8 X Kappm the dependence of transhydrogenase rate on the value of the membrane potential (zero pH gradient) was determined at pH 6.3, 6.9, 7.6 and 9.0. The relation was similar at pH 6.9 and 7.6. At alkaline pH the apparent threshold in the relation became more prominent as it was shifted to slightly higher values of membrane potential. At acid pH a shift in the opposite direction diminished the apparent threshold and saturation at high membrane potential became more dominant. We use these data in an attempt to discriminate between two models of energy transduction: (a) the driving force exerted by the membrane potential is mediated by a pH gradient formed through the operation of a proton well in the transhydrogenase; (b) the membrane potential increases a rate constant for charge translocation through transhydrogenase by decreasing the effective height of the Eyring barrier for charge transfer across the membrane through the enzyme. The second model leads to a more simple description than the first of the pH dependence of transhydrogenase rate on membrane potential.4+ transhydrogenase activity in chromatopho

Bacteria↗
PubMed1989

In vitro effects of endotoxin on bovine and sheep lung microvascular and pulmonary artery endothelial cells.

A single infusion of Escherichia coli endotoxin into sheep results in structural evidence of pulmonary endothelial injury, increases in both prostacyclin and prostaglandin E2 (PGE2) in lung lymph, and an increase in pulmonary microvascular permeability. Endotoxin-induced lung endothelial damage can also be induced in vitro, but to date these studies have utilized endothelium from large pulmonary vessels. In the present study, we have grown endothelial cells from peripheral lung vessels of cows and sheep and exposed these microvascular endothelial cells to endotoxin. Controls included lung microvascular endothelium without endotoxin and endothelial cells from bovine and sheep main pulmonary artery with and without addition of endotoxin. We found that endotoxin caused significant increases in release of prostacyclin and PGE2 from both bovine and sheep lung microvascular and pulmonary artery endothelium. Normal bovine and sheep pulmonary artery and bovine lung microvascular endothelium released greater levels of prostacyclin than PGE2 (ng/ng); release of PGE2 from the microvascular cells was greater than from the pulmonary artery endothelium in both species. Exposure of endothelial cells from cow and sheep main pulmonary artery to endotoxin results in endothelial cell retraction and pyknosis, a loss of barrier function, increased release of prostacyclin and PGE2 and eventual cell lysis. In lung microvascular cells, the increases in prostanoids were accompanied by changes in cell shape but occurred in the absence of either detectable alterations in barrier function or cytolysis. Thus, while endotoxin causes alterations to endothelial cells from both large and small pulmonary vessels, the effects are not identical suggesting site specific phenotypic expression of endothelial cells even within a single vessel. To determine whether the response of either the large or small pulmonary vessel endothelial cells in culture mimics most closely the in vivo response of the lung to endotoxin requires further study.

Animals↗
PubMed1989

Human recombinant interleukin 2-activated sheep lymphocytes lyse sheep pulmonary microvascular endothelial cells.

Administration of lymphokine-activated killer (LAK) cells in combination with interleukin 2 (IL-2) has been effective in reducing tumor mass in humans, but has been accompanied by significant toxicity. We used a chronic awake sheep model to investigate the cause of the vascular leak syndrome associated with IL-2 administration. Sheep repeatedly infused with human recombinant IL-2 (hrIL-2) developed mild pulmonary hypertension, systemic hypotension, acidemia, hypoxemia, and increased flow of protein rich lung lymph. We hypothesized that LAK cells may damage lung endothelium in vivo and cause increased lung vascular permeability. Sheep peripheral blood and lung lymph lymphocytes incubated in vitro with hrIL-2 generated cytotoxic activity for human K-562 cells and sheep pulmonary microvascular endothelial cells. In addition, cytotoxic effector cells were isolated from the peripheral blood of a sheep which had received hrIL-2. These observations suggest that LAK cells possess the ability to damage endothelial cells and may contribute to an increased pulmonary vascular permeability observed following hrIL-2 infusion in sheep.

Animals↗
PubMed1989

The extracellular matrix in large-cell lymphomas: a histopathologic, immunohistochemical, and ultrastructural study.

We studied the histopathologic, immunohistochemical, and ultrastructural features of the extracellular matrix (ECM) in 20 immunologically defined large-cell lymphomas, including immunoblastic sarcoma of B cells (three patients), peripheral T cell lymphoma (five patients), large non-cleaved follicular center cell (FCC) lymphoma (nine patients), and non-marking large-cell lymphoma (three patients). Immunohistochemical studies were performed with antibodies to laminin, fibronectin, and collagen types I, III, IV, and V. The immunologically defined subgroups demonstrated characteristic differences in ECM in light microscopic appearance, composition, and ultrastructural features. Immunoblastic sarcomas of B cells showed delicate intercellular bands that were apparent only at high power but were distinct in exhibiting focal staining for basement membrane elements (laminin and type IV collagen) in addition to type I collagen and fibronectin. Electron microscopically, no basal lamina were apparent, although the collagen fibers were embedded in a dense matrix not seen in the other lymphomas. All peripheral T cell lymphomas exhibited a packeting pattern of intercellular bands and were distinguished by the frequent presence of intense pericellular staining for type V collagen as well as by focal pericellular staining for types I and III collagen. The latter finding corresponded to extensive areas of direct contact between tumor cells and the ECM by electron microscopy. The large non-cleaved FCC lymphomas and the non-marking large-cell lymphomas demonstrated both diffuse and compartmentalizing arrangements of intercellular bands that frequently coexisted and stained predominantly for fibronectin and types I and III collagen. All groups demonstrated myofibroblasts and fibroblasts partially or completely separating the ECM from tumor cells, suggesting that most of the ECM is part of a reaction to these lymphomas. These studies show more variation in light microscopic appearance, composition, and ultrastructural relationships of the intercellular and pericellular ECM than was apparent in earlier studies of cleaved FCC lymphomas.

Aged↗